Today, Dr. Mike Eades has a fascinating article on his ProteinPower Blog, Ketosis cleans our cells.
It's one of those "must read" items of the day - so without further ado, go...go read it!
Tuesday, February 28, 2006
Monday, February 27, 2006
Low-Fat May Increase Relative Risk for Cardiovascular Events
Back in 2003, researchers decided to see how good the DASH Diet is compared to the Standard American Diet. They designed a twelve-week trial with a two-week run-in where the diet over those two weeks contained 37% total fat with 16% of calories from saturated fat. With 100 subjects participating, 50 were randomized to consume the DASH Diet while the other 50 were on their own to eat as they wished - this second group was the "control group."
This particular study was well-designed - it not only sought to investigate the impact of diet on cholesterol levels, but also C-Reactive Protein (CRP), a marker of inflammation in the body that we understand is a pretty good predictor of cardiovascular risk - more so than cholesterol levels.The DASH Diet really modified what the intervention group ate. Their diet contained just 27% total fat and just 6% saturated fat.
So, what happened after three months on this "better" diet?
Not much in the way of benefit. In fact, some findings were downright scary and the conclusions in the abstract only hint at how poorly some on the DASH Diet fared compared to the control group, "the presence of increased CRP was associated with less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet. These findings document an additional mechanism by which inflammation might increase cardiovascular disease risk."
Notice, the researchers don't say anything in their conclusions about how we might need to re-think our dietary recommendations, especially in those with elevated CRP levels? How about I show you what happened, what the data actually tells us?
First, here is the full-text of the article Inflammation modifies the effects of a reduced-fat low-cholesterol diet on lipids: results from the DASH-sodium trial.
Those placed on the DASH Diet had median baseline cholesterol levels
Total Cholesterol = 204.3
LDL Cholesterol = 131
HDL Cholesterol = 48.7
Triglycerides = 89.48
TC/HDL Ratio = 4.2LDL/HDL Ratio = 2.6
When the group was divided into those who had a baseline CRP below or above the median the results were indicative of how damaging a low-fat diet can be:
For those with CRP below the median CRP of 2.37 the following happened:
Total Cholesterol = 176.47
LDL Cholesterol = 110.29
HDL Cholesterol = 45.66
Triglycerides = 90.37
TC/HDL Ratio = 3.86
LDL/HDL Ratio = 2.4
No one can argue - they did pretty good. Not blow your socks off impressive, but they didn't get appear to get worse and their TC/HDL and LDL/HDL Ratios did improve slightly. Keep in mind though, the diet did nothing to reduce their level of CRP though. We'll get to that in a moment. For now, let's see how those with CRP levels above the median fared...
Total Cholesterol = 201.63
LDL Cholesterol = 130.03
HDL Cholesterol = 46.44
Triglycerides = 110.75
TC/HDL Ratio = 4.34
LDL/HDL Ratio = 2.8
This "unfavorable outcome" on these subjects' health occured in just three months and the best the researchers could do is bury it in the full-text rather than make it very clear in their abstract that the difference isn't just the minor inconvenience of "less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet" but statistically significant differences that had real potential to negatively impact health if such changes continued with eating such a diet over the long-term.
Not only did the diet result in an "unfavorable outcome" for these individuals, but when it did not change their CRP level that means that this change increased their relative risk for a cardiovascular event - basically increased their risk to have a heart attack.
Let's explore why the CRP levels were important here - not just for those with above the median levels, but also those below the median. First, the researchers interpretation that those with CRP below the group median had a favorable outcome with the diet is misleading in my opinion. While the diet did have an effect on cholesterol levels and ratios, it had NO EFFECT on the CRP levels of the subjects following the DASH Diet.
The abstract states this "The DASH diet, net of control, had no effect on CRP."
If we use Ridker et al's assessment of risk, developed in the New England Journal of Medicine publication of Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events, we find that the baseline risk of those assigned the DASH Diet was a relative risk of 2.9. That is, when they started the DASH Diet they already had a 2.9 times greater risk of a cardiovascular event than someone with a "normal" CRP value of 1.6 or less. Let me be clear here - 1.6 may even be considered high if we use the Framingham data as a benchmark, but for now, let's stick with the Ridker et al method to assess risk.
Because their CRP didn't change, even the change in their cholesterol and TC/HDL didn't improve their relative risk. It actually made it worse! We must consider that the diet did not change their CRP level when determining risk here and use the value they used - 2.37. In Ridker et al's assessment protocol, that level combined with a TC/HDL ratio of 3.86 translates to a relative risk of 3.5 times greater risk of a cardiovascular event than someone with a "normal" CRP value of 1.6 or less. Did you catch that? The relative risk increased from 2.9 to 3.5!
For those who had a CRP above the median, we again must maintain no change in CRP from baseline as the data suggests. Here, the change in risk is dramatic because the TC/HDL Ratio changed so much. For those eating the DASH Diet who had a CRP above the median, the resultant change in their TC/HDL Ratio increased their relative risk to a 4.2 times greater risk of a cardiovascular event than someone with a "normal" CRP of 1.6 or less. Their relative risk increased from 2.9 to 4.2!
Let me be clear here - Ridker et al published their work almost a year before this DASH Diet trial - yet the researchers didn't even consider discussing the implications of the findings in terms of relative risk. Instead they couched their words with phrases like "less favorable" and "likely relationship" between diet and lipids without any real fear the DASH Diet might not just cause an "unfavorable" outcome in terms of lipid values (cholesterol readings) but real world problems, like an increased relative risk for cardiovascular events!
Ridker et al aren't the only ones to find such a disturbing relationship with CRP and relative risk either!
In October 2001, the International Journal of Obesity and Related Metabolic Disorders published findings from Pannacciulli et al, C-reactive protein is independently associated with total body fat, central fat, and insulin resistance in adult women. Their findings - Our study has shown an independent relationship of central fat accumulation and insulin resistance with CRP plasma levels, thus suggesting that mild, chronic inflammation may be a further component of the metabolic syndrome and a mediator of the atherogenic profile of this syndrome. [I chose this particular study as an example because those who followed the DASH Diet had a mean BMI of 29.3 - they were bordering on obese and had elevated CRP levels!]
In June 2001, the journal Atherosclerosis, published The association of c-reactive protein, serum amyloid a and fibrinogen with prevalent coronary heart disease--baseline findings of the PAIS project, which concluded that "CRP, SAA and fibrinogen, which are markers of inflammation, were positively and significantly associated with prevalent CHD."
So the concept that CRP is a valuable marker and when measured should be used as part of an assessment of risk isn't really a stretch here. The researchers failed to acknowledge its potential importance, the increased relative risk even in those with CRP below their baseline measure and especially in those with CRP above their baseline measure. Their simple conclusion that some realize less benefit from the DASH diet totally fails to recognize that neither group reduced their relative risk for a cardiovascular event - in fact, both groups had an increased risk after three months - one group moreso than the other - but both still increased their risk!
And now, some three years later, with even more trials completed, even more data showing the same miserable effects, we're still being told that DASH and other low fat dietary approaches are better for us!
Better than what? Perhaps better at increasing relative risk?
The data shows they're no better or worse than the Standard American Diet - which I'm sure you'll agree is certainly not leading us to better health and quality of life long-term. So then, what exactly is a low-fat diet better than since almost every trial is comparing it to the Standard American Diet? I know I'd like to know.
We're told it's better, but for some reason no one can tell what it's better than - and don't forget we're not told about the risks to many of us from these "better" diets - risks that are clear as day when you look at the data and not just rely on the basic information in the abstract! Not a peep from the AHA about this finding or any caution about how this dietary approach - DASH - may really negatively affect someone with a high CRP level.
Don't you think it's time we took this stuff seriously and actually looked for a dietary approach that works as promised - ya know, one that does optimize health and well-being over the long-term, that does reduce the risk of disease and premature death and that is based on evidence instead of prevailing dogma?
This particular study was well-designed - it not only sought to investigate the impact of diet on cholesterol levels, but also C-Reactive Protein (CRP), a marker of inflammation in the body that we understand is a pretty good predictor of cardiovascular risk - more so than cholesterol levels.The DASH Diet really modified what the intervention group ate. Their diet contained just 27% total fat and just 6% saturated fat.
So, what happened after three months on this "better" diet?
Not much in the way of benefit. In fact, some findings were downright scary and the conclusions in the abstract only hint at how poorly some on the DASH Diet fared compared to the control group, "the presence of increased CRP was associated with less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet. These findings document an additional mechanism by which inflammation might increase cardiovascular disease risk."
Notice, the researchers don't say anything in their conclusions about how we might need to re-think our dietary recommendations, especially in those with elevated CRP levels? How about I show you what happened, what the data actually tells us?
First, here is the full-text of the article Inflammation modifies the effects of a reduced-fat low-cholesterol diet on lipids: results from the DASH-sodium trial.
Those placed on the DASH Diet had median baseline cholesterol levels
Total Cholesterol = 204.3
LDL Cholesterol = 131
HDL Cholesterol = 48.7
Triglycerides = 89.48
TC/HDL Ratio = 4.2LDL/HDL Ratio = 2.6
When the group was divided into those who had a baseline CRP below or above the median the results were indicative of how damaging a low-fat diet can be:
For those with CRP below the median CRP of 2.37 the following happened:
Total Cholesterol = 176.47
LDL Cholesterol = 110.29
HDL Cholesterol = 45.66
Triglycerides = 90.37
TC/HDL Ratio = 3.86
LDL/HDL Ratio = 2.4
No one can argue - they did pretty good. Not blow your socks off impressive, but they didn't get appear to get worse and their TC/HDL and LDL/HDL Ratios did improve slightly. Keep in mind though, the diet did nothing to reduce their level of CRP though. We'll get to that in a moment. For now, let's see how those with CRP levels above the median fared...
Total Cholesterol = 201.63
LDL Cholesterol = 130.03
HDL Cholesterol = 46.44
Triglycerides = 110.75
TC/HDL Ratio = 4.34
LDL/HDL Ratio = 2.8
This "unfavorable outcome" on these subjects' health occured in just three months and the best the researchers could do is bury it in the full-text rather than make it very clear in their abstract that the difference isn't just the minor inconvenience of "less total and LDL cholesterol reduction and a greater increase in triglycerides from a reduced-fat/low-cholesterol diet" but statistically significant differences that had real potential to negatively impact health if such changes continued with eating such a diet over the long-term.
Not only did the diet result in an "unfavorable outcome" for these individuals, but when it did not change their CRP level that means that this change increased their relative risk for a cardiovascular event - basically increased their risk to have a heart attack.
Let's explore why the CRP levels were important here - not just for those with above the median levels, but also those below the median. First, the researchers interpretation that those with CRP below the group median had a favorable outcome with the diet is misleading in my opinion. While the diet did have an effect on cholesterol levels and ratios, it had NO EFFECT on the CRP levels of the subjects following the DASH Diet.
The abstract states this "The DASH diet, net of control, had no effect on CRP."
If we use Ridker et al's assessment of risk, developed in the New England Journal of Medicine publication of Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events, we find that the baseline risk of those assigned the DASH Diet was a relative risk of 2.9. That is, when they started the DASH Diet they already had a 2.9 times greater risk of a cardiovascular event than someone with a "normal" CRP value of 1.6 or less. Let me be clear here - 1.6 may even be considered high if we use the Framingham data as a benchmark, but for now, let's stick with the Ridker et al method to assess risk.
Because their CRP didn't change, even the change in their cholesterol and TC/HDL didn't improve their relative risk. It actually made it worse! We must consider that the diet did not change their CRP level when determining risk here and use the value they used - 2.37. In Ridker et al's assessment protocol, that level combined with a TC/HDL ratio of 3.86 translates to a relative risk of 3.5 times greater risk of a cardiovascular event than someone with a "normal" CRP value of 1.6 or less. Did you catch that? The relative risk increased from 2.9 to 3.5!
For those who had a CRP above the median, we again must maintain no change in CRP from baseline as the data suggests. Here, the change in risk is dramatic because the TC/HDL Ratio changed so much. For those eating the DASH Diet who had a CRP above the median, the resultant change in their TC/HDL Ratio increased their relative risk to a 4.2 times greater risk of a cardiovascular event than someone with a "normal" CRP of 1.6 or less. Their relative risk increased from 2.9 to 4.2!
Let me be clear here - Ridker et al published their work almost a year before this DASH Diet trial - yet the researchers didn't even consider discussing the implications of the findings in terms of relative risk. Instead they couched their words with phrases like "less favorable" and "likely relationship" between diet and lipids without any real fear the DASH Diet might not just cause an "unfavorable" outcome in terms of lipid values (cholesterol readings) but real world problems, like an increased relative risk for cardiovascular events!
Ridker et al aren't the only ones to find such a disturbing relationship with CRP and relative risk either!
In October 2001, the International Journal of Obesity and Related Metabolic Disorders published findings from Pannacciulli et al, C-reactive protein is independently associated with total body fat, central fat, and insulin resistance in adult women. Their findings - Our study has shown an independent relationship of central fat accumulation and insulin resistance with CRP plasma levels, thus suggesting that mild, chronic inflammation may be a further component of the metabolic syndrome and a mediator of the atherogenic profile of this syndrome. [I chose this particular study as an example because those who followed the DASH Diet had a mean BMI of 29.3 - they were bordering on obese and had elevated CRP levels!]
In June 2001, the journal Atherosclerosis, published The association of c-reactive protein, serum amyloid a and fibrinogen with prevalent coronary heart disease--baseline findings of the PAIS project, which concluded that "CRP, SAA and fibrinogen, which are markers of inflammation, were positively and significantly associated with prevalent CHD."
So the concept that CRP is a valuable marker and when measured should be used as part of an assessment of risk isn't really a stretch here. The researchers failed to acknowledge its potential importance, the increased relative risk even in those with CRP below their baseline measure and especially in those with CRP above their baseline measure. Their simple conclusion that some realize less benefit from the DASH diet totally fails to recognize that neither group reduced their relative risk for a cardiovascular event - in fact, both groups had an increased risk after three months - one group moreso than the other - but both still increased their risk!
And now, some three years later, with even more trials completed, even more data showing the same miserable effects, we're still being told that DASH and other low fat dietary approaches are better for us!
Better than what? Perhaps better at increasing relative risk?
The data shows they're no better or worse than the Standard American Diet - which I'm sure you'll agree is certainly not leading us to better health and quality of life long-term. So then, what exactly is a low-fat diet better than since almost every trial is comparing it to the Standard American Diet? I know I'd like to know.
We're told it's better, but for some reason no one can tell what it's better than - and don't forget we're not told about the risks to many of us from these "better" diets - risks that are clear as day when you look at the data and not just rely on the basic information in the abstract! Not a peep from the AHA about this finding or any caution about how this dietary approach - DASH - may really negatively affect someone with a high CRP level.
Don't you think it's time we took this stuff seriously and actually looked for a dietary approach that works as promised - ya know, one that does optimize health and well-being over the long-term, that does reduce the risk of disease and premature death and that is based on evidence instead of prevailing dogma?
Of Mice and Men
An interesting study was published in the Proceedings of the National Academy of Sciences from researchers at Oregon Health & Science University who discovered that removing a gene involved in repairing damaged DNA causes mice to develop the metabolic syndrome.
The findings were the subject of the article, Removing DNA Repair Gene Causes Metabolic Syndrome, published in Genomics and Proteomics last week.
Those of you who are frequent readers of my column know I am cautious about trying to extrapolate findings from animal models to make a case for why things happen in humans. This finding however, is fascinating. Indeed, it may open the door to truly understanding what is happening in the metabolism of a person developing and eventually presenting with metabolic syndrome - characterized by the following features: obesity, hypertension, dislipidemia (high LDL and triglycerides with low HDL), insulin resistance and high blood sugars.
This study is the first to link DNA repair with the metabolic syndrome, and the findings suggest an important role for what is the "NEIL1 gene product" in the prevention of the diseases associated with the disorder, including obesity, hypertension, high cholesterol, insulin resistance and kidney disease. R. Stephen Lloyd, PhD, senior scientist at OHSU's Center for Research on Occupational and Environmental Toxicology (CROET) and co-author of the study said that "...if there are catalytically compromised forms of NEIL1 within the U.S. population, these people will be predicted to be at increased risk for developing the metabolic syndrome," a disease believed to affect more than 40 million Americans. Lloyd and his colleagues originally discovered the NEIL1-deficient mouse's propensity for developing the metabolic disorder about two years ago.
Where this gets really interesting is in the explanation of what happens when this piece of DNA is lacking or damaged.
"If you have oxidative stress inside the cell, then the bases in the DNA can become damaged, and the responsibility of this whole group of enzymes is essentially to monitor the entire genome, looking for genomic bases that have been oxidatively damaged," Lloyd explained. "They have the responsibility of then removing the damaged bases, which initiates a process by which the cell puts in a normal piece of DNA where the damaged DNA was. This happens every second of your life."
Llyod and his colleague, the study's lead author, Vladimir Vartanian, PhD, created "knock-out" mice - animals bred to lack the NEIL1 gene. Hold on to your hat - here is where the rubber meets the road of this finding - the researchers found that "the mice lacking the enzyme reached weights of between 45 and 52 grams at age 7 months, while normal mice weighed in at only 28 grams. They also were extremely lethargic, their hair was turning gray, and some were even going bald. And there were gender differences." The male mice had more severe presentation of the features of Metabolic Syndrome, at an earlier age, than the female mice did.
"This means mutations in the NEIL1 gene, or the gene's absence altogether, could have a catastrophic effect on the body's ability to restore DNA to its undamaged state."
"Our analysis is that the inability to repair damage to the genetic material, whether it is in the nucleus or whether it's in the mitochondria, is what's leading to a destabilization of a normal metabolic process," Lloyd said. "That then begins to cascade and ultimately results in the symptoms that are consistent with the metabolic syndrome."
Those last two quotes from the article are critical to our understanding of just how devastating damage to our DNA is. And, while the researchers are eager to continue with research into this particular gene to figure out how to develop a screening test for humans, I think there is enough solid understanding about what potentially damages our DNA and how to try to prevent or reverse such damage.
We must eat foods rich in nutrients - those that provide us with a full range of antioxidants - and ensure we're eating adequate protein for our essential amino acids, along with quality fats and oils for our essential fatty acid requirements and requirement for fat soluable vitamins. While the above study was indeed only mice - the finding that a piece of the DNA missing or damaged has such a profound effect metabolically, that is it causes Metabolic Syndrome, should be setting off alarms bells in the research community!
Later today, I'm even going to show you that researchers have had warning bells going off for years in their data but have ignored it as they continue to desperately prove a low-fat diet is optimal for health. This while more and more people are presenting with Metabolic Syndrome, Insulin Resistance and Diabetes!
The findings were the subject of the article, Removing DNA Repair Gene Causes Metabolic Syndrome, published in Genomics and Proteomics last week.
Those of you who are frequent readers of my column know I am cautious about trying to extrapolate findings from animal models to make a case for why things happen in humans. This finding however, is fascinating. Indeed, it may open the door to truly understanding what is happening in the metabolism of a person developing and eventually presenting with metabolic syndrome - characterized by the following features: obesity, hypertension, dislipidemia (high LDL and triglycerides with low HDL), insulin resistance and high blood sugars.
This study is the first to link DNA repair with the metabolic syndrome, and the findings suggest an important role for what is the "NEIL1 gene product" in the prevention of the diseases associated with the disorder, including obesity, hypertension, high cholesterol, insulin resistance and kidney disease. R. Stephen Lloyd, PhD, senior scientist at OHSU's Center for Research on Occupational and Environmental Toxicology (CROET) and co-author of the study said that "...if there are catalytically compromised forms of NEIL1 within the U.S. population, these people will be predicted to be at increased risk for developing the metabolic syndrome," a disease believed to affect more than 40 million Americans. Lloyd and his colleagues originally discovered the NEIL1-deficient mouse's propensity for developing the metabolic disorder about two years ago.
Where this gets really interesting is in the explanation of what happens when this piece of DNA is lacking or damaged.
"If you have oxidative stress inside the cell, then the bases in the DNA can become damaged, and the responsibility of this whole group of enzymes is essentially to monitor the entire genome, looking for genomic bases that have been oxidatively damaged," Lloyd explained. "They have the responsibility of then removing the damaged bases, which initiates a process by which the cell puts in a normal piece of DNA where the damaged DNA was. This happens every second of your life."
Llyod and his colleague, the study's lead author, Vladimir Vartanian, PhD, created "knock-out" mice - animals bred to lack the NEIL1 gene. Hold on to your hat - here is where the rubber meets the road of this finding - the researchers found that "the mice lacking the enzyme reached weights of between 45 and 52 grams at age 7 months, while normal mice weighed in at only 28 grams. They also were extremely lethargic, their hair was turning gray, and some were even going bald. And there were gender differences." The male mice had more severe presentation of the features of Metabolic Syndrome, at an earlier age, than the female mice did.
"This means mutations in the NEIL1 gene, or the gene's absence altogether, could have a catastrophic effect on the body's ability to restore DNA to its undamaged state."
"Our analysis is that the inability to repair damage to the genetic material, whether it is in the nucleus or whether it's in the mitochondria, is what's leading to a destabilization of a normal metabolic process," Lloyd said. "That then begins to cascade and ultimately results in the symptoms that are consistent with the metabolic syndrome."
Those last two quotes from the article are critical to our understanding of just how devastating damage to our DNA is. And, while the researchers are eager to continue with research into this particular gene to figure out how to develop a screening test for humans, I think there is enough solid understanding about what potentially damages our DNA and how to try to prevent or reverse such damage.
We must eat foods rich in nutrients - those that provide us with a full range of antioxidants - and ensure we're eating adequate protein for our essential amino acids, along with quality fats and oils for our essential fatty acid requirements and requirement for fat soluable vitamins. While the above study was indeed only mice - the finding that a piece of the DNA missing or damaged has such a profound effect metabolically, that is it causes Metabolic Syndrome, should be setting off alarms bells in the research community!
Later today, I'm even going to show you that researchers have had warning bells going off for years in their data but have ignored it as they continue to desperately prove a low-fat diet is optimal for health. This while more and more people are presenting with Metabolic Syndrome, Insulin Resistance and Diabetes!
Friday, February 24, 2006
Anthony Colpo - Why the Low-Fat Diet is Stupid and Potentially Dangerous
For years Anthony Colpo has maintained The Omnivore, a website bursting at the seams with articles and insights into studies and claims about being healthy - all with references to studies.
This week, Colpo penned "Why the Low-Fat Diet is Stupid and Potentially Dangerous" - a lengthy and well referenced article about the null findings from the Women's Health Initiative Dietary Modification Trial.
Today, it's featured here, in its entirety with permission to reprint. Colpo has an amusing disclaimer at the end - you'll probably want to read it before sending him an email if you want to communicate with him!
Why the Low-Fat Diet is Stupid and Potentially Dangerous
Anthony Colpo, February 23, 2006
On February 8, 2006, the Journal of the American Medical Association delivered a huge blow to advocates of low-fat 'nutrition' by publishing the results of the huge Women's Health Initiative trial. The results of the trial clearly showed that a low-fat diet failed to prevent cardiovascular disease or cancer in women even when followed continuously for eight years. In women with pre-existing CVD, the low-fat diet increased the risk of CVD by 26 percent!
Since the publication of the WHI results, low-fat diet supporters have been working overtime manufacturing excuses for the failure of their beloved regimen. Foremost among these is that the women in the low-fat group did not reduce their fat intake sufficiently. I even had one sadly misguided soul write to me the other day telling me I did not "understand" low-fat diets, that the only reason they frequently fail is because people following them don't lower their fat intake enough.
Such stupidity makes my head spin…
First of all, I understand low-fat diets only too well! Much to my regret, I followed one throughout most of the nineties, and the result was nothing short of disastrous.
My low-fat nightmare began in my early twenties, after a doctor told me that my cholesterol, at 213, was "moderately high" and placed me at increased risk of heart disease (something I now know to be nonsense). Following the prevailing dietary wisdom at the time, I soon adopted a low-fat diet. This wasn't your average low-fat diet--it was a VERY low-fat diet, with the kind of anemic fat intake that would have made lipid-phobes like Ornish and Pritikin proud.
For years, I ate only the leanest meats; in fact, to this day, the thought of eating another skinless chicken breast, kangaroo steak, or low-fat fish makes me want to puke! Fuelling the high energy demands of my daily workouts in the face of a low fat intake meant eating carbohydrates--lots of them! In keeping with the common advice still given to athletes to eat lots of 'healthy' complex carbohydrate foods, I consumed copious amounts of rye bread, brown rice, sweet potato, wholemeal pasta, rolled oats, buckwheat, and millet.
My dedication to the low-fat mantra was nothing short of religious, and my low-fat brainwashing so thorough that when I sat down and calculated the average amount of fat calories I was taking in, I was actually proud when I realized I was consistently consuming less than ten percent of my calories as fat every day!
Halfway through the nineties, reality began to bite--hard. Despite my 'healthy' diet, and my daily strenuous training regimen, my blood pressure had risen from 110/65, a reading characteristic of highly-conditioned athletes, to an elevated 130/90. I noticed it was becoming increasingly harder to maintain the lean, "ripped", vascular look that I had always prided myself on. Instead, my physique was becoming increasingly smooth and bloated. My digestive system became progressively more sluggish, my stomach often feeling heavy and distended after meals. I frequently felt tired after meals. I showed signs of leaky gut syndrome, racking up a rather impressive list of irreversible food sensitivities. I had never been much of a coffee drinker, but I was now frequently trying to fight off increasing fatigue by sipping a strong black or two before training sessions. My fasting blood glucose level was below the normal range, indicative of reactive hypoglycemia.
Basically, I felt like crap!
It wasn't until I abandoned the whole low-fat charade, and adopted a diet that went against everything preached by the reigning diet orthodoxy, that I began to reverse these symptoms. When I ate more saturated fat and meat than ever before and subsequently felt better than ever before, I quickly realized that most diet 'experts' actually had no clue what they were talking about. I quickly realized that they were mere parrots repeating an official party line.
When I look back on my fat-fearing days, where I really believed that dietary fat was some sort of heinous toxin, the first thought that comes to mind is "What a wanker!" I then think of the sad legion of brainwashed folks all around the world who still follow the idiotic low-fat paradigm. "Poor folks," I think to myself, "they really have no idea just how badly they've been had…"
While I feel sorry for many of these folks, I have nothing but utter contempt for those who write me in defense of the low-fat paradigm. To be fooled is one thing, but to vigorously defend those who have mercilessly deceived and shafted you is beyond pitiful--such self-destructive stupidity is an absolutely repugnant thing to observe!
Let's now find out why the participants in the diet group of the WHI trial should be glad that they did not lower their fat intake any more than what they did!
Why the Low-Fat Diet is a Big Fat Fraud
One of the first priorities of healthy eating is to consume the most nutrient-dense foods possible. Cutting your fat intake strongly impedes this goal via at least three mechanisms:
1) Directly slashing your intake of important vitamins and fatty acids;2) Reducing the absorption of crucial fat-soluble vitamins;3) Decreasing the absorption of important minerals.
You probably think you're being "enlightened" when you trim the fat from your meats and ditch your egg yolks down the sink. What you are really doing is lucidly demonstrating what a mindless, brainwashed dolt you've become. You are effectively throwing away nutrients that your body needs to survive and thrive!
The fatty portions of meat, dairy and eggs are where one finds the highest concentrations of fat-soluble vitamins such as A, D, E and beta-carotene. Stripping the skin from your chicken breast not only makes it less tasty, but reduces its vitamin A content by seventy-eight percent!(1)
Throwing away your egg yolks is equally dumb. While one large egg yolk contains 245 IU of vitamin A, 18 IU of vitamin D, and 186 mcg of lutein plus zeaxanthin, along with small amounts of other carotenoids and vitamin E, a large egg white contains none of these nutrients. Egg yolks, along with beef liver, are also an especially concentrated dietary source of phosphatidylcholine (lecithin) and choline, which the body requires for healthy liver function and for the formation of the key neurotransmitter acetylcholine. Lower levels of acetylcholine are associated with memory loss and cognitive decline(2).
The last time you chose skim milk yogurt instead of the whole milk variety, you nutritionally short-changed yourself; skim yogurt contains 93 percent less vitamin A than whole yogurt! And if you chose non-fat yogurt, then congratulations--you received no vitamin A whatsoever!(1)
Data from national nutrition surveys consistently show that American children have lower than recommended intakes of vitamin E, and this is reflected in below-average serum levels of the vitamin. Reduction in dietary fat further exacerbates the low vitamin E status of children(3). The consequences of low dietary vitamin E intakes may include impaired immune responses, and an increased susceptibility to cardiovascular disease and cancer.
Willingly reducing your consumption of important vitamins and carotenes is not smart--it's downright stupid!
Absorb This!
Low-fat eating doesn't just decrease your intake of certain crucial nutrients. As researchers have shown time and time again, it will also dramatically reduce the absorption of whatever fat-soluble vitamins and carotenes remain in your diet!(4-7).
When subjects ingested equal amounts of lutein--a carotenoid that may protect against age-related macular degeneration and cataract--from either whole eggs, spinach or supplements, it was observed that lutein absorption was significantly higher during the period of whole egg consumption(8).
In another study, researchers compared the absorption of carotenoids from salads that contained either 0, 6 or 28 grams of canola oil. There was no increase in blood carotenoid concentrations after the fat-free salad, while the reduced fat salad produced markedly lower blood carotenoid elevations than the high fat version(9).
The addition of 150 grams of fat-rich avocado to salsa enhanced lycopene and beta-carotene absorption by 4.4 and 2.6-fold, respectively, compared to avocado-free salsa. In the same subjects, adding either twenty-four grams of avocado oil or 150 grams avocado to salad greatly enhanced alpha-carotene, beta -carotene and lutein absorption by 7.2, 15.3 and 5.1 times, respectively, compared with avocado-free salad!(10)
Only a true dumbass would think that reducing absorption of healthful fat-soluble nutrients is somehow beneficial. Don't be a dumbass.
Making a Bad Situation Worse
The mineral status of the typical Westerner is atrocious. Take magnesium for example, a substance vital for healthy heart function, blood sugar control, bone formation, and muscular contraction(11-16). A recent survey of U.S. adults found that the average daily intake of magnesium among Caucasian men is only 352 milligrams, and a mere 278 milligrams among African American men. Caucasian women consume an average of 256 milligrams per day, while African American women take in only 202 milligrams daily(17). The lower amounts of magnesium ingested by African Americans have been posited as a possible contributor to their increased susceptibility of hypertension, diabetes, and cardiovascular disease(18).
The situation isn't much better for zinc. Overt zinc deficiencies are common to Third World countries where animal protein consumption is low, while milder, 'sub-clinical' zinc deficiencies appear to be common in modernized nations. Nationwide food consumption surveys by the USDA have found that the average intake of zinc for males and females of all ages is below the recommended daily allowance (RDA). This is especially worrying when one considers that RDAs are generally based on the amount of a nutrient required to prevent obvious, well-recognized deficiency diseases (such as stunted growth and hypogonadism in the case of zinc), not sub-clinical deficiencies that may damage one's health over the longer-term.
Those who follow low fat diets are at even greater risk of zinc deficiency(19,20). Not only do low-fat diets discourage the consumption of zinc-rich foods like red meat, but a low dietary fat intake itself acts to impair mineral absorption.
It's ironic that red meat is typically denigrated for its saturated fat content, because saturates are the very fats that improve mineral absorption!(21-24).
A pilot study by researchers at the USDA Grand Forks Human Nutrition Research Center examined the effect of different fats and carbohydrate on performance and mineral metabolism in three male endurance cyclists. During alternating four-week periods, each subject consumed diets in which either carbohydrate, polyunsaturated, or saturated fat contributed about fifty percent of daily energy intake. Endurance capacity decreased with the polyunsaturated fat diet. The polyunsaturated diet also resulted in increased excretion of zinc and iron, while copper retention tended to be positive only on the saturated fat diet(25).
Optimal health is next to impossible to achieve with sub-optimal mineral status. Low-fat diets, most notably those low in saturated fats, encourage sub-optimal mineral status. Yet another reason why these diets suck the salsiccia, big time!
Low-Fat, Low Omega-3
Unless you've been living on a distant planet for the last few years, then you have no doubt heard about omega-3 fats and their pivotal role in maintaining good health.
Unlike low-fat diets, clinical trials utilizing the sole intervention of increased fatty fish or fish oil intake have produced significant reductions in CHD and overall mortality. The benefits of EPA and DHA-rich items like fish and fish oil are not confined to the cardiovascular system. In epidemiological studies and animal experiments, increased intakes of long-chain omega-3 fatty acids have been associated with lower rates of cancer, depression and mental illness, adverse pregnancy outcomes, infectious disease, osteoporosis, lung disease, menstrual pain, cognitive decline in the elderly, eye damage, childhood asthma and attention-deficit hyperactivity disorder(26-51). In clinical trials with human subjects, researchers have observed benefits from long-chain omega-3 supplementation in the treatment of asthma, alzheimers, rheumatoid arthritis, depression, schizophrenia, infant health, pregnancy outcomes, kidney disease, menstrual problems, ulcerative colitis, Crohn's disease and cystic fibrosis(52-73). Hell, even the fat-hating vegetarian Dean Ornish recommends the use of distinctly non-vegetarian fish oil supplements! (Gee, can anyone see a contradiction there?)
So what has this all got to do with low-fat eating? Everything!
Similar to fat-soluble vitamins, the absorption of EPA and DHA increases when consumed with a high fat meal(74).
Again, not just any old fat will do when it comes to improving one's omega-3 status. Saturated fat improves the body's conversion of plant-source omega-3 fats into the longer-chain varieties EPA and DHA, while omega-6-rich fats impede the conversion process. In young males, elongation of alpha-linolenic acid (ALA) and linoleic acid (LA) to DHA, EPA and AA was reduced by forty to fifty percent when dietary LA intake increased from fifteen to thirty grams per day(75).
When rats were supplemented with linseed oil, their serum and tissue content of the all-important omega-3 fatty acids increased, and omega-6 levels decreased, to a far greater extent on a saturated fat-rich (beef fat) diet than on a linoleic acid-rich (safflower oil) diet(76).
Cutting fat--as in saturated fat--worsens your omega-3 status. If you think that's a good thing, then low-fat nutrition has already scrambled your brain. My advice: Eat some fat before you become totally brain dead!
Speaking of scrambled brains…
Nature's Anti-Depressant: Fat!
Feeling moody? Irritable? Always snapping at your kids for no good reason? Are you known around the office as "Attila the Grump"? If so, eating a low-fat diet isn't going to help the situation. In fact, a low-fat diet may actually be the cause of your mental funk!
In 1998, U.K. researchers reported the results of an important experiment involving twenty healthy male and female volunteers. One group was placed on a 41% fat diet, while the other group consumed a 25% fat diet. After 4 weeks had passed, the groups were swapped around so that those originally on the low-fat diet were now consuming the high-fat diet, and vice-versa. Throughout the study, all meals were prepared by the university conducting the study and supplied to the participants. Both diets were specially designed to be as palatable and similar in taste as possible.
At the beginning and end of each diet period, every subject underwent a battery of psychological assessments, including various mood state questionnaires and an interview by a psychiatrist who was blinded to the participant's dietary status.
The study was tightly-controlled and adherence to the diets appears to have been high. HDL cholesterol levels declined during the low-fat period, a typical response on low-fat, high-carb diets, indicating that subjects ate the foods as supplied.
The researchers found that, while ratings of anger-hostility slightly declined during the high-fat diet period, they significantly increased during the low-fat, high-carb diet period!
Tension-anxiety ratings declined during the high-fat period, but did not change during the four weeks of low-fat, high-carb eating.
Ratings of depression declined slightly during the high-fat period, but increased during the low-fat, high-carb period, mainly due to two of the low-fat subjects reporting significantly greater depression-dejection ratings.
What is particularly alarming about this study is that the low-fat diet produced these symptoms in mentally healthy subjects. As the researchers emphasized, the participants were "a psychologically robust group who had never previously suffered from depression or anxiety, and who were not going through any 'stressful' events during the study." They further stated that "The alterations in mood observed in the present study may have been greater if subjects were feeling more stressed or were more susceptible to mental illness."(77)
Low-fat diets should be approached with extreme caution by those with a history of depression, anxiety, overly aggressive behavior or mental illness. Such individuals may be especially vulnerable to the nutritional inadequacies of low-fat diets.
The UK researchers' observations raise some interesting questions. Could the low-fat, high-carbohydrate diets that have been so heavily promoted over the last thirty years be at least partially responsible for increases in anti-social behavior witnessed during the same period? If studies with our primate cousins are anything to go by, the answer to this question could well be affirmative.
Low-Fat Diet Makes Monkeys Go Ape
For almost 2 years, adult male monkeys were fed a "luxury" diet - (43% calories from fat, 0.34 mg cholesterol/Calorie of diet) or a "prudent" diet (30% calories from fat, 0.05 mg cholesterol/Calorie of diet).
Researchers observed that the low-fat diet monkeys were more irritable and initiated more aggression than the "luxury" diet animals.
The prudent diet resulted in lower total serum cholesterol levels, something that our absent-minded health authorities automatically assume is a good thing. The researchers, however, noted: "These results are consistent with studies linking relatively low serum cholesterol concentrations to violent or antisocial behavior in psychiatric and criminal populations and could be relevant to understanding the significant increase in violence-related mortality observed among people assigned to cholesterol-lowering treatment in clinical trials."(78)
A research monkey after discovering he was going to be placed on a low-fat diet for almost 2 years.
Fatless Shrugged
It was Ayn Rand who once said that the most noble and productive goal for a person to engage in was the pursuit of their own happiness. If the achievement of your own happiness is important to you, then kick the low-fat diet's sad, sorry, melancholy butt right out of your life--it's a loser.
Low-Fat Diets Lower Testosterone
Testosterone is abhorred by politically correct weenies, who like to blame it for every instance of disagreeable male behavior, in much the same way menstruation was once cited as the catch-all explanation for uncharacteristically aggressive or irritable female behavior.
Of course, scientific reality is of little concern to the politically correct. The fact is, testosterone is an extremely important hormone for both men and women. Sex drive, muscle and bone health, immune function, cognitive function, mood, and cardiovascular health are all negatively affected by declining levels of testosterone. Testosterone levels typically decline with age, and, along with the decline of other key hormones, falling T levels are believed to be a major contributor to many of the deleterious changes seen during the aging process. As such, aging individuals should be looking at ways to preserve and even boost their testosterone status, rather than engaging in self-defeating habits that will speed the decline in T levels. Alcohol abuse, recreational drug use, pharmaceutical drugs, stress, and poor sleep habits can all lower testosterone levels.
So too can low-fat diets.
Research shows that reducing fat intake from around forty percent to 20-25 percent of calories decreases testosterone output. Low fat diets also increase levels of sex hormone-binding globulin (SHBG), a protein which binds to testosterone, thus reducing the amount of bioavailable, or 'free', testosterone in the body. It is free testosterone that is responsible for this hormone's favorable effects on growth, repair, sexual capacity and immune function(79-81).
Again, not just any old fat will suffice when it comes to optimizing testosterone levels. A study with weight-training men showed higher saturated fat and monounsaturated fat consumption to be positively associated with testosterone levels. In contrast, higher dietary levels of so-called "heart-healthy" polyunsaturated fats relative to saturated fats were associated with lower testosterone levels (82).
It's highly ironic that athletes and bodybuilders will take all manner of expensive, esoteric and often dubious testosterone-boosting concoctions--not to mention anabolic steroids--yet will follow hormone-damping low-fat diets with religious fervor. It's a little like putting on a weighted vest before a big race and expecting to run at full speed.
Hormones like testosterone play a fundamentally important role in stimulating and regulating growth and metabolism. Don't go throwing a low-fat monkey wrench into your metabolic engine!
Low-Fat Diets and Immune Function
Diet 'experts' assure us that a low-fat diet is the key to good health. The published research does not support such claims.
Despite the virulent ranting of anti-fat activists, trials comparing sedentary adult volunteers fed low-fat diets with those receiving higher fat diets has shown no improvement in immune status in the former group(83,84).
In children, whole milk consumption is associated with fewer gastrointestinal infections than consumption of low fat milk (85). Rats consuming diets high in milk fat show a significantly greater resistance to Listeria infection and higher survival rates than those whose diets were low in milk fat(86). Similar results have been observed in mice fed diets high in saturate-rich coconut oil(87)
In athletes, who are constantly pushing their immune systems to the edge with strenuous training, adherence to the commonly-recommended low-fat high-carbohydrate diet (15-19% of total calories) increases pro-inflammatory immune factors, decreases anti-inflammatory factors, and depresses antioxidant status when compared to higher fat diets (30-50% of total calories)(88,89). Such changes may leave athletes on low-fat diets with a lowered resistance to infection and a higher risk of chronic illness. This may be due to difficulty in obtaining sufficient calories from low-fat diets to meet the energy demands of exercise; increasing dietary fat intake and total caloric intake to match energy expenditure appears to reverse the negative effects on immune function reported on calorie-deficient, low-fat diets. Diets comprising 32% to 55% fat also improve endurance capacity compared to diets with 15% fat(90).
It was Scandinavian researchers who, in the 1960s, performed research showing that using extremely high-carbohydrate, low-fat diets for short periods could enhance athletic performance. This was achieved by using these diets as part of a "depletion-repletion" carbohydrate-loading strategy, which helped temporarily elevate muscle glycogen stores to higher than usual levels. One of the pioneers in this area, Dr. Jan Karlsson, points out that such diets were never intended to be applied for more than 3-4 days. Karlsson and his colleagues openly lament that these diets are now employed for extended periods of time, and refer to the prolonged use of very high-carbohydrate/low-fat diets by athletes as "voluntary malnourishment". They note that in Scandinavia, researchers use the term "Carbohydrate Trap" when referring to the widespread belief that these diets are required for optimal performance. These researchers consider a 50-55% carbohydrate, 35% fat diet to be eminently more sensible and nutritious than the >60% carb, <25% fat diets commonly used by athletes(91).
For athletes and non-athletes alike, the low-fat diet is a sick (pun intended) joke.
The Low-Fat Diet Does Not Protect Against Heart Disease, and May Actually Worsen It
The WHI trial confirmed what well-read cholesterol skeptics have known for a long time: The low-fat diet is a big fat fraud when it comes to preventing heart disease. Among the 48,835 women participating in the trial, no significant differences in CHD or stroke incidence, CHD or stroke mortality, or total mortality were observed(92). Nor were there any reductions in the incidence or mortality rates of breast cancer, colorectal cancer, or total cancer(93,94).
There was however, one very ominous finding to emerge from the WHI trial. Among the 3.4 percent of trial participants with pre-existing cardiovascular disease, those randomized to the low-fat diet experienced a 26% increase in the relative risk of non-fatal and fatal CHD!
Low-fat advocates have remained deafeningly silent on this inconvenient finding, and would no doubt like to believe this was just a 'freak' occurrence. However, this is hardly the first time that low-fat eating has been shown to worsen the prognosis of women with existing cardiovascular disease.
In 2004, the world's most prominent nutrition journal, The American Journal of Clinical Nutrition, published the results of a very, very interesting study. Harvard researchers had taken 235 postmenopausal women with established coronary heart disease, and divided them into four categories according to their level of saturated fat intake. They then performed coronary angiographies at baseline and after a mean follow-up of 3.1 years, analyzing over 2,200 coronary artery segments in the process.
After adjusting for multiple confounders, a higher saturated fat intake was associated with less narrowing of the arteries and less progression of coronary atherosclerosis. Compared with a 0.22 mm narrowing in the lowest quartile of intake, there was a 0.10-mm narrowing in the second quartile, a 0.07 mm narrowing in the third quartile, and no narrowing in the fourth and highest quartile of saturated fat intake!
Following a low-fat diet means adopting a high-carbohydrate diet by default. After all, it is exceedingly difficult and highly unpalatable to achieve the bulk of one's caloric needs by eating lean protein foods. It is of no small concern then, that carbohydrate intake was positively associated with atherosclerotic progression, particularly when the glycemic index was high. The intake of so-called 'heart-healthy' polyunsaturated fats was also positively associated with progression of atherosclerosis, but monounsaturated and total fat intakes were not associated with progression (it must be noted that the major sources of polyunsaturates in Western countries are refined vegetable oils which are rich in the omega-6 fat linoleic acid. The polyunsaturated omega-3 fats, which are underconsumed by most Westerners, have actually been shown to lower CVD).
After examining the baseline data for the study subjects, it is apparent that the results can not be explained away by otherwise healthier lifestyles among those eating the most saturated fat; the high saturated fat group, in fact, had the greatest number of current smokers! Women eating the most saturated fat were also less likely to take blood-thinning medications like aspirin(95).
If this study had found saturated fats to be associated with cardiovascular disease, its results would have been trumpeted in headlines around the world. Instead, they were largely ignored by the mainstream media and our ever-so responsible 'health' authorities. It appears only studies that support the cherished dogma of our health orthodoxy are considered suitable as press release fodder…
A major factor in the progression of cardiovascular disease--and most major diseases--is free radical damage. It is well-established that saturated fatty acids, because of their lack of vulnerable double bonds, are the least susceptible to free radical damage; polyunsaturates are the most vulnerable. We also know that increased carbohydrate consumption, especially of the refined variety, does an outstanding job of raising blood sugar and insulin levels, which accelerates glycation, free radical activity, blood clot formation, and arterial smooth muscle cell proliferation.
It should also be noted that increasing heart disease incidence throughout the twentieth century has been accompanied by increasing polyunsaturate consumption, while a marked increase in refined carbohydrate consumption during the last three decades has been accompanied by spiralling obesity and diabetes incidence. Animal fat consumption, in contrast, has remained stable over the last 100 years.
So what we have is two studies that show that women with pre-existing heart disease will experience WORSE outcomes if they shun saturated fat and opt for a low-fat/high-carbohydrate diet! Furthermore, the validity of these results is supported by basic biochemistry and epidemiological data. So will low-fat advocates stop recommending this pattern of eating to women with heart disease? Does their concern for human life override their need to defend their precious low-fat dogma at all costs?
I truly doubt it…
If low-fat advocates won't be straight with you, then I will. Let's be perfectly clear on this: If you are female, and suffer cardiovascular disease, the published, peer-reviewed scientific evidence indicates that adopting a low-fat diet could be DEADLY.
The WHI is not the only dietary intervention trial to demonstrate the worthlessness of the low-fat diet in preventing CVD. In 1965, the prominent journal Lancet published the results of a trial conducted by the UK Medical Research Committee. In this study, 264 men under 65 were assigned to either a low-fat diet or their usual diet. Dietary records show that those in the low-fat group averaged 45 g/day of fat throughout the trial, while those in the control group actually increased their average fat intake from 106 to 125g. The average serum cholesterol measurement of the low-fat group was 25 points lower than that of the control group at 4 years. Despite nonsensical claims that "every 1mg/dl drop in cholesterol equals a 2% drop in CHD risk", there were no differences between the two groups in CHD incidence or mortality after 4 years.
In Search of the Elusive 'Negative Fat Intake'!
The hysterical anti-fat vitriole that spews forth from some anti-fat faddists leads me to believe that if these clowns could eat a 'negative-fat' diet, they would! As for their argument that the above trials didn't lower fat enough, one has to wonder how creating even greater deficiencies in valuable nutrients, and predisposing one to greater risk of depression and anger--all of which low-fat diets have indeed been clinically documented to do--will in any way help prevent heart disease! Maybe these folks have been eating low-fat so long that it's started to drain their brains; healthy human brains, after all, are 60% fat by weight!
The authors of the MRC trial concluded that: "A low-fat diet has no place in the treatment of myocardial infarction." Despite being written over forty years ago, these words have largely been ignored by a medical and health hierarchy which seems to earnestly believe that if only it keeps flogging the dead low-fat horse, it will one-day magically spring to life. In Australia, this is known as engaging in a 'wank', which means that people who push low-fat diets despite no proof whatsoever of their efficacy are wankers. This might be stating the obvious, but…you really shouldn't listen to wankers!
But the Japanese Eat a Low-Fat Diet…Don't They?
Supporters of low-fat nutrition cite the Japanese ad nauseum, claiming that their low-fat/high-carbohydrate diet is the reason for their low rate of heart disease. It is ironic that many of these same commentators exhort the benefits of whole-grains and tell us that the only 'bad' carbohydrates are those that come from refined sugars and grains. These folks need to get their story straight---a major source of carbohydrates in the Japanese diet is white rice--a refined grain! That means that if the high-carbohydrate Japanese diet is cardio-protective, then refined grains must be good for one's heart! Well, which is it? You can't have it both ways; either refined grains are heart-friendly, or they're not!
The truth is, the longevity and low CHD incidence of the Japanese owes nothing to carbohydrate intake, refined or otherwise. During the 1960s and 1970s, industrialization underwent rapid growth in Japan. This period of marked economic change bought with it greater consumption of animal protein and fat. This increased animal food consumption in Japan has been accompanied by a marked decline in both the overall incidence of and the mortality from one of that nation's biggest killers--stroke. This increase in animal protein and animal fat consumption has also occurred alongside Japan's rise to the top of the longevity ladder.(96,97)
If you're tempted to write this off as merely a consequence of improved living standards and medical technology, keep in mind that long-term follow-up studies with both native and migrant Japanese populations show that those who eat the most animal protein and animal fat enjoy greater longevity and a lower incidence of stroke than those who eat lesser amounts(98-101).
OK, So What About the Mediterranean Diet?
A diet low in saturated fat is purportedly a major factor in the low rates of CHD observed in Southern European countries. Just one wee problem: France, the Mediterranean country with the lowest CHD rates of all, is also the Mediterranean country with the highest saturated fat intake!
Oops!
Health 'experts' have tried to brush off this embarrassing observation as a 'paradox' (orthodoxy loves applying the 'paradox' label to uncomfortable contradictions) by claiming that red wine explains this difference. If that were true, then the Italians, who drink a similar amount of red wine, should have CHD rates even lower than France. But they don't; their CHD rates are similar to those of other Southern European countries where far less red wine is consumed(102).
Conclusion
I could go on, and on, and on…but I'll just close by saying that the low-fat diet has NEVER been demonstrated to do all the wonderful health-fortifying things claimed for it. The only trials showing favorable effects in people following low-fat diets are those that simultaneously employed other truly useful interventions, like exercise, stress management, increased fruit and vegetable intake and decreased processed food intake, and weight loss. However, there is absolutely no law whatsoever stating that low-fat eating is required for the implementation of any of these strategies. In fact, given the available evidence, one can only conclude that the inclusion of higher fat intakes in these trials may even have improved the results!
The bottom line: Not only is low-fat eating a boring way to go through life, it is a useless and often counterproductive hoax.
References and Assorted Disclaimers:
DISGRUNTLED WORSHIPPERS OF THE LOW-FAT RELIGION SHOULD READ THE FOLLOWING:I have not stated anything in this article that cannot be verified by published, peer-reviewed research. Nonetheless, my inbox will no doubt be flooded with angry emails from those who have been brainwashed by the low-fat paradigm, and who violently object to the thought that something that they have believed in so strongly for so long might actually be false. In other words, malevolent dimwits who want to shoot the messenger! For those of you who fall into this category, my suggestions are as follows: 1) GROW UP!; 2) Start placing a premium on discovering the facts, as opposed to doggedly defending what you have already decided you want to believe; 3) Instead of attacking me, start questioning the motives of those who profit greatly from the fallacious anti-fat, anti-cholesterol paradigm. This includes the food and drug conglomerates that make BILLIONS from the sale of low-fat foods and cholesterol-lowering drugs, the health and dietetic 'associations/organizations/institutes/foundations/etc' who receive millions in 'donations' from these very same companies, and the executives of these so-called 'non-profit' organizations who enjoy six-figure incomes and extensive perquisites.
To attack the owner of a non-commercial web site, who has nothing to gain financially by either supporting or opposing the low-fat paradigm, while defending those WHO DO, is so bloody stupid that it defies comprehension. Unfortunately, there are a lot of bloody stupid people in the world! If you are one of them, and decide to write me, please note that unless your email contains valid references to the scientific literature, it will be deleted immediately. After having established yourself as an ignorant goofball, your email address will also be added to my spam filter and any further emails will be delivered straight to my trash. Sorry, but I really am extremely busy and have no time or patience for ignorant, time-wasting twits.
NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first)! However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part. A hyperlink to www.TheOmnivore.com would also be greatly appreciated! Those wishing to reprint this or any other article on TheOmnivore.com for commercial purposes should email: ac.theomnivore@gmail.com
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61. Jorgensen MH, et al. Effect of formula supplemented with docosahexaenoic acid and gamma-linolenic acid on fatty acid status and visual acuity in term infants. Journal of Pediatric Gastroenterology and Nutrition, 1998; 26: 412-421.
62. Carlson SE, et al. Visual acuity and fatty acid status of term infants fed human milk and formulas with and without docosahexaenoate and arachidonate from egg yolk lecithin. Pediatric Research, 1996; 39: 882-888.
63. O'Connor DL, et al. Growth and Development in Preterm Infants Fed Long-Chain Polyunsaturated Fatty Acids: A Prospective, Randomized Controlled Trial. Pediatrics, Aug 1, 2001; 108 (2): 359-371.
64. Helland IB, et al. Maternal Supplementation With Very-Long-Chain n-3 Fatty Acids During Pregnancy and Lactation Augments Children's IQ at 4 Years of Age. Pediatrics, Jan, 2003; 111 (1): e39-e44.
65. Dunstan JA, et al. Fish oil supplementation in pregnancy modifies neonatal allergen-specific immune responses and clinical outcomes in infants at high risk of atopy: a randomized, controlled trial. Journal of Allergy and Clinical Immunology, Dec, 2003; 112 (6): 1178-1184.
66. Olsen SF, et al. Randomised controlled trial of effect of fish-oil supplementation on pregnancy duration. Lancet, Apr 25, 1992; 339 (8800): 1003-1007.
67. Olsen SF, Secher NJ. A possible preventive effect of low-dose fish oil on early delivery and pre-eclampsia: indications from a 50-year-old controlled trial. British Journal of Nutrition, Nov, 1990; 64 (3): 599-609.
68. De Caterina R et al. n-3 fatty acids and renal diseases. American Journal of Kidney Diseases, Sept, 1994; 24 (3): 397-415.
69. Harel Z et al. Supplementation with omega-3 polyunsaturated fatty acids in the management of dysmenorrhea in adolescents. American Journal of Obstetrics & Gynecology, Apr, 1996; 174 (4): 1335-1338.
70. Aslan A, Triadafilopoulos G. Fish oil fatty acid supplementation in active ulcerative colitis: A double-blind, placebo-controlled, crossover study. American Journal of Gastroenterology, Apr, 1992; 87: 432-37.
71. Salomon, P., et al. Treatment of ulcerative colitis with fish oil n-3 omega fatty acid: an open trial. Journal of Clinical Gastroenterology, Apr, 1990; (12): 157-1161.
72. Belluzzi A et al. Effect of an enteric-coated fish-oil preparation on relapses in Crohn's disease. New England Journal of Medicine, Jun 13, 1996; 334 (24): 1557-1560.
73. Lawrence R, Sorrell T. Eicosapentaenoic acid in cystic fibrosis: evidence of a pathogenetic role for leukotriene B4. Lancet, Aug 21, 1993; 342: 465-469.
74. Lawson LD, Hughes BG. Absorption of eicosapentaenoic acid and docosahexaenoic acid from fish oil triacylglycerols or fish oil ethyl esters co-ingested with a high-fat meal. Biochem Biophys Res Commun, Oct 31, 1988; 156 (2): 960-963.
75. Emken EA, et al. Dietary linoleic acid influences desaturation and acylation of deuterium-labeled linoleic and linolenic acids in young adult males. Biochim Biophys Acta, Aug 4, 1994; 1213 (3): 277-288.
76. Garg ML, et al. Dietary saturated fat level alters the competition between alpha-linolenic and linoleic acid. Lipids 1989 Apr;24(4): 334-339.
77. Wells AS, et al. Alterations in mood after changing to a low-fat diet. British Journal of Nutrition, Jan, 1998; 79 (1): 23-30.
78. Kaplan JR, et al. The effects of fat and cholesterol on social behavior in monkeys. Psychosom Med. 1991 Nov-Dec; 53 (6): 634-642.
79. Hamalainen EK, et al. Decrease of serum total and free testosterone during a low-fat high-fibre diet. J Steroid Biochem. Mar 1983; 18 (3): 369-370.
80. Reed MJ, et al. Dietary lipids: an additional regulator of plasma levels of sex hormone binding globulin. J. Clin. Endocrinol. Metab, 1987; 64: 1083-1085.
81. Dorgan JF, et al. Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. Am J Clin Nutr. Dec 1996; 64 (6): 850-855.
82. Volek JS, et al. Testosterone and cortisol in relationship to dietary nutrients and resistance exercise. Journal of Applied Physiology, Jan 1997; 82 (1): 49-54.
83. Kelley DS, et al. Energy restriction decreases number of circulating natural killer cells and serum levels of immunoglobulins in overweight women. European Journal of Clinical Nutrition, Jan, 1994; 48 (1): 9-18.
84. van het Hof KH, et al. A long-term study on the effect of spontaneous consumption of reduced fat products as part of a normal diet on indicators of health. International Journal of Food Sciences and Nutrition, Jan, 1997; 48 (1): 19-29.
85. Koopman JS, et al. Milk fat and gastrointestinal illness. Am. J. Public Health 1984; 74: 1371-1373
86. Puertollano MA, et al. Relevance of Dietary Lipids as Modulators of Immune Functions in Cells Infected with Listeria monocytogenes. Clinical and Diagnostic Laboratory Immunology, Mar. 2002; 9 (2): 352-357.
87. de Pablo MA, et al. Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes. FEMS Immunol Med Microbiol. 2000 Feb;27(2):127-33.
88. Meksawan K, et al. Effect of dietary fat intake and exercise on inflammatory mediators of the immune system in sedentary men and women. Journal of the American College of Nutrition, Aug, 2004; 23 (4): 331-340.
89. Venkatraman JT, et al. Dietary fats and immune status in athletes: clinical implications. Medicine and Science in Sports and Exercise, Jul, 2000; 32 (7 Suppl): S389-S395.
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92. Howard BV, et al. Low-Fat Dietary Pattern and Risk of Cardiovascular Disease: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 655-666.
93. Prentice RL, et al. Low-Fat Dietary Pattern and Risk of Invasive Breast Cancer: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 629-642.
94. Beresford SAA, et al. Low-Fat Dietary Pattern and Risk of Colorectal Cancer: The Women's Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, Feb 8, 2006; 295: 643-654.
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This week, Colpo penned "Why the Low-Fat Diet is Stupid and Potentially Dangerous" - a lengthy and well referenced article about the null findings from the Women's Health Initiative Dietary Modification Trial.
Today, it's featured here, in its entirety with permission to reprint. Colpo has an amusing disclaimer at the end - you'll probably want to read it before sending him an email if you want to communicate with him!
Why the Low-Fat Diet is Stupid and Potentially Dangerous
Anthony Colpo, February 23, 2006
On February 8, 2006, the Journal of the American Medical Association delivered a huge blow to advocates of low-fat 'nutrition' by publishing the results of the huge Women's Health Initiative trial. The results of the trial clearly showed that a low-fat diet failed to prevent cardiovascular disease or cancer in women even when followed continuously for eight years. In women with pre-existing CVD, the low-fat diet increased the risk of CVD by 26 percent!
Since the publication of the WHI results, low-fat diet supporters have been working overtime manufacturing excuses for the failure of their beloved regimen. Foremost among these is that the women in the low-fat group did not reduce their fat intake sufficiently. I even had one sadly misguided soul write to me the other day telling me I did not "understand" low-fat diets, that the only reason they frequently fail is because people following them don't lower their fat intake enough.
Such stupidity makes my head spin…
First of all, I understand low-fat diets only too well! Much to my regret, I followed one throughout most of the nineties, and the result was nothing short of disastrous.
My low-fat nightmare began in my early twenties, after a doctor told me that my cholesterol, at 213, was "moderately high" and placed me at increased risk of heart disease (something I now know to be nonsense). Following the prevailing dietary wisdom at the time, I soon adopted a low-fat diet. This wasn't your average low-fat diet--it was a VERY low-fat diet, with the kind of anemic fat intake that would have made lipid-phobes like Ornish and Pritikin proud.
For years, I ate only the leanest meats; in fact, to this day, the thought of eating another skinless chicken breast, kangaroo steak, or low-fat fish makes me want to puke! Fuelling the high energy demands of my daily workouts in the face of a low fat intake meant eating carbohydrates--lots of them! In keeping with the common advice still given to athletes to eat lots of 'healthy' complex carbohydrate foods, I consumed copious amounts of rye bread, brown rice, sweet potato, wholemeal pasta, rolled oats, buckwheat, and millet.
My dedication to the low-fat mantra was nothing short of religious, and my low-fat brainwashing so thorough that when I sat down and calculated the average amount of fat calories I was taking in, I was actually proud when I realized I was consistently consuming less than ten percent of my calories as fat every day!
Halfway through the nineties, reality began to bite--hard. Despite my 'healthy' diet, and my daily strenuous training regimen, my blood pressure had risen from 110/65, a reading characteristic of highly-conditioned athletes, to an elevated 130/90. I noticed it was becoming increasingly harder to maintain the lean, "ripped", vascular look that I had always prided myself on. Instead, my physique was becoming increasingly smooth and bloated. My digestive system became progressively more sluggish, my stomach often feeling heavy and distended after meals. I frequently felt tired after meals. I showed signs of leaky gut syndrome, racking up a rather impressive list of irreversible food sensitivities. I had never been much of a coffee drinker, but I was now frequently trying to fight off increasing fatigue by sipping a strong black or two before training sessions. My fasting blood glucose level was below the normal range, indicative of reactive hypoglycemia.
Basically, I felt like crap!
It wasn't until I abandoned the whole low-fat charade, and adopted a diet that went against everything preached by the reigning diet orthodoxy, that I began to reverse these symptoms. When I ate more saturated fat and meat than ever before and subsequently felt better than ever before, I quickly realized that most diet 'experts' actually had no clue what they were talking about. I quickly realized that they were mere parrots repeating an official party line.
When I look back on my fat-fearing days, where I really believed that dietary fat was some sort of heinous toxin, the first thought that comes to mind is "What a wanker!" I then think of the sad legion of brainwashed folks all around the world who still follow the idiotic low-fat paradigm. "Poor folks," I think to myself, "they really have no idea just how badly they've been had…"
While I feel sorry for many of these folks, I have nothing but utter contempt for those who write me in defense of the low-fat paradigm. To be fooled is one thing, but to vigorously defend those who have mercilessly deceived and shafted you is beyond pitiful--such self-destructive stupidity is an absolutely repugnant thing to observe!
Let's now find out why the participants in the diet group of the WHI trial should be glad that they did not lower their fat intake any more than what they did!
Why the Low-Fat Diet is a Big Fat Fraud
One of the first priorities of healthy eating is to consume the most nutrient-dense foods possible. Cutting your fat intake strongly impedes this goal via at least three mechanisms:
1) Directly slashing your intake of important vitamins and fatty acids;2) Reducing the absorption of crucial fat-soluble vitamins;3) Decreasing the absorption of important minerals.
You probably think you're being "enlightened" when you trim the fat from your meats and ditch your egg yolks down the sink. What you are really doing is lucidly demonstrating what a mindless, brainwashed dolt you've become. You are effectively throwing away nutrients that your body needs to survive and thrive!
The fatty portions of meat, dairy and eggs are where one finds the highest concentrations of fat-soluble vitamins such as A, D, E and beta-carotene. Stripping the skin from your chicken breast not only makes it less tasty, but reduces its vitamin A content by seventy-eight percent!(1)
Throwing away your egg yolks is equally dumb. While one large egg yolk contains 245 IU of vitamin A, 18 IU of vitamin D, and 186 mcg of lutein plus zeaxanthin, along with small amounts of other carotenoids and vitamin E, a large egg white contains none of these nutrients. Egg yolks, along with beef liver, are also an especially concentrated dietary source of phosphatidylcholine (lecithin) and choline, which the body requires for healthy liver function and for the formation of the key neurotransmitter acetylcholine. Lower levels of acetylcholine are associated with memory loss and cognitive decline(2).
The last time you chose skim milk yogurt instead of the whole milk variety, you nutritionally short-changed yourself; skim yogurt contains 93 percent less vitamin A than whole yogurt! And if you chose non-fat yogurt, then congratulations--you received no vitamin A whatsoever!(1)
Data from national nutrition surveys consistently show that American children have lower than recommended intakes of vitamin E, and this is reflected in below-average serum levels of the vitamin. Reduction in dietary fat further exacerbates the low vitamin E status of children(3). The consequences of low dietary vitamin E intakes may include impaired immune responses, and an increased susceptibility to cardiovascular disease and cancer.
Willingly reducing your consumption of important vitamins and carotenes is not smart--it's downright stupid!
Absorb This!
Low-fat eating doesn't just decrease your intake of certain crucial nutrients. As researchers have shown time and time again, it will also dramatically reduce the absorption of whatever fat-soluble vitamins and carotenes remain in your diet!(4-7).
When subjects ingested equal amounts of lutein--a carotenoid that may protect against age-related macular degeneration and cataract--from either whole eggs, spinach or supplements, it was observed that lutein absorption was significantly higher during the period of whole egg consumption(8).
In another study, researchers compared the absorption of carotenoids from salads that contained either 0, 6 or 28 grams of canola oil. There was no increase in blood carotenoid concentrations after the fat-free salad, while the reduced fat salad produced markedly lower blood carotenoid elevations than the high fat version(9).
The addition of 150 grams of fat-rich avocado to salsa enhanced lycopene and beta-carotene absorption by 4.4 and 2.6-fold, respectively, compared to avocado-free salsa. In the same subjects, adding either twenty-four grams of avocado oil or 150 grams avocado to salad greatly enhanced alpha-carotene, beta -carotene and lutein absorption by 7.2, 15.3 and 5.1 times, respectively, compared with avocado-free salad!(10)
Only a true dumbass would think that reducing absorption of healthful fat-soluble nutrients is somehow beneficial. Don't be a dumbass.
Making a Bad Situation Worse
The mineral status of the typical Westerner is atrocious. Take magnesium for example, a substance vital for healthy heart function, blood sugar control, bone formation, and muscular contraction(11-16). A recent survey of U.S. adults found that the average daily intake of magnesium among Caucasian men is only 352 milligrams, and a mere 278 milligrams among African American men. Caucasian women consume an average of 256 milligrams per day, while African American women take in only 202 milligrams daily(17). The lower amounts of magnesium ingested by African Americans have been posited as a possible contributor to their increased susceptibility of hypertension, diabetes, and cardiovascular disease(18).
The situation isn't much better for zinc. Overt zinc deficiencies are common to Third World countries where animal protein consumption is low, while milder, 'sub-clinical' zinc deficiencies appear to be common in modernized nations. Nationwide food consumption surveys by the USDA have found that the average intake of zinc for males and females of all ages is below the recommended daily allowance (RDA). This is especially worrying when one considers that RDAs are generally based on the amount of a nutrient required to prevent obvious, well-recognized deficiency diseases (such as stunted growth and hypogonadism in the case of zinc), not sub-clinical deficiencies that may damage one's health over the longer-term.
Those who follow low fat diets are at even greater risk of zinc deficiency(19,20). Not only do low-fat diets discourage the consumption of zinc-rich foods like red meat, but a low dietary fat intake itself acts to impair mineral absorption.
It's ironic that red meat is typically denigrated for its saturated fat content, because saturates are the very fats that improve mineral absorption!(21-24).
A pilot study by researchers at the USDA Grand Forks Human Nutrition Research Center examined the effect of different fats and carbohydrate on performance and mineral metabolism in three male endurance cyclists. During alternating four-week periods, each subject consumed diets in which either carbohydrate, polyunsaturated, or saturated fat contributed about fifty percent of daily energy intake. Endurance capacity decreased with the polyunsaturated fat diet. The polyunsaturated diet also resulted in increased excretion of zinc and iron, while copper retention tended to be positive only on the saturated fat diet(25).
Optimal health is next to impossible to achieve with sub-optimal mineral status. Low-fat diets, most notably those low in saturated fats, encourage sub-optimal mineral status. Yet another reason why these diets suck the salsiccia, big time!
Low-Fat, Low Omega-3
Unless you've been living on a distant planet for the last few years, then you have no doubt heard about omega-3 fats and their pivotal role in maintaining good health.
Unlike low-fat diets, clinical trials utilizing the sole intervention of increased fatty fish or fish oil intake have produced significant reductions in CHD and overall mortality. The benefits of EPA and DHA-rich items like fish and fish oil are not confined to the cardiovascular system. In epidemiological studies and animal experiments, increased intakes of long-chain omega-3 fatty acids have been associated with lower rates of cancer, depression and mental illness, adverse pregnancy outcomes, infectious disease, osteoporosis, lung disease, menstrual pain, cognitive decline in the elderly, eye damage, childhood asthma and attention-deficit hyperactivity disorder(26-51). In clinical trials with human subjects, researchers have observed benefits from long-chain omega-3 supplementation in the treatment of asthma, alzheimers, rheumatoid arthritis, depression, schizophrenia, infant health, pregnancy outcomes, kidney disease, menstrual problems, ulcerative colitis, Crohn's disease and cystic fibrosis(52-73). Hell, even the fat-hating vegetarian Dean Ornish recommends the use of distinctly non-vegetarian fish oil supplements! (Gee, can anyone see a contradiction there?)
So what has this all got to do with low-fat eating? Everything!
Similar to fat-soluble vitamins, the absorption of EPA and DHA increases when consumed with a high fat meal(74).
Again, not just any old fat will do when it comes to improving one's omega-3 status. Saturated fat improves the body's conversion of plant-source omega-3 fats into the longer-chain varieties EPA and DHA, while omega-6-rich fats impede the conversion process. In young males, elongation of alpha-linolenic acid (ALA) and linoleic acid (LA) to DHA, EPA and AA was reduced by forty to fifty percent when dietary LA intake increased from fifteen to thirty grams per day(75).
When rats were supplemented with linseed oil, their serum and tissue content of the all-important omega-3 fatty acids increased, and omega-6 levels decreased, to a far greater extent on a saturated fat-rich (beef fat) diet than on a linoleic acid-rich (safflower oil) diet(76).
Cutting fat--as in saturated fat--worsens your omega-3 status. If you think that's a good thing, then low-fat nutrition has already scrambled your brain. My advice: Eat some fat before you become totally brain dead!
Speaking of scrambled brains…
Nature's Anti-Depressant: Fat!
Feeling moody? Irritable? Always snapping at your kids for no good reason? Are you known around the office as "Attila the Grump"? If so, eating a low-fat diet isn't going to help the situation. In fact, a low-fat diet may actually be the cause of your mental funk!
In 1998, U.K. researchers reported the results of an important experiment involving twenty healthy male and female volunteers. One group was placed on a 41% fat diet, while the other group consumed a 25% fat diet. After 4 weeks had passed, the groups were swapped around so that those originally on the low-fat diet were now consuming the high-fat diet, and vice-versa. Throughout the study, all meals were prepared by the university conducting the study and supplied to the participants. Both diets were specially designed to be as palatable and similar in taste as possible.
At the beginning and end of each diet period, every subject underwent a battery of psychological assessments, including various mood state questionnaires and an interview by a psychiatrist who was blinded to the participant's dietary status.
The study was tightly-controlled and adherence to the diets appears to have been high. HDL cholesterol levels declined during the low-fat period, a typical response on low-fat, high-carb diets, indicating that subjects ate the foods as supplied.
The researchers found that, while ratings of anger-hostility slightly declined during the high-fat diet period, they significantly increased during the low-fat, high-carb diet period!
Tension-anxiety ratings declined during the high-fat period, but did not change during the four weeks of low-fat, high-carb eating.
Ratings of depression declined slightly during the high-fat period, but increased during the low-fat, high-carb period, mainly due to two of the low-fat subjects reporting significantly greater depression-dejection ratings.
What is particularly alarming about this study is that the low-fat diet produced these symptoms in mentally healthy subjects. As the researchers emphasized, the participants were "a psychologically robust group who had never previously suffered from depression or anxiety, and who were not going through any 'stressful' events during the study." They further stated that "The alterations in mood observed in the present study may have been greater if subjects were feeling more stressed or were more susceptible to mental illness."(77)
Low-fat diets should be approached with extreme caution by those with a history of depression, anxiety, overly aggressive behavior or mental illness. Such individuals may be especially vulnerable to the nutritional inadequacies of low-fat diets.
The UK researchers' observations raise some interesting questions. Could the low-fat, high-carbohydrate diets that have been so heavily promoted over the last thirty years be at least partially responsible for increases in anti-social behavior witnessed during the same period? If studies with our primate cousins are anything to go by, the answer to this question could well be affirmative.
Low-Fat Diet Makes Monkeys Go Ape
For almost 2 years, adult male monkeys were fed a "luxury" diet - (43% calories from fat, 0.34 mg cholesterol/Calorie of diet) or a "prudent" diet (30% calories from fat, 0.05 mg cholesterol/Calorie of diet).
Researchers observed that the low-fat diet monkeys were more irritable and initiated more aggression than the "luxury" diet animals.
The prudent diet resulted in lower total serum cholesterol levels, something that our absent-minded health authorities automatically assume is a good thing. The researchers, however, noted: "These results are consistent with studies linking relatively low serum cholesterol concentrations to violent or antisocial behavior in psychiatric and criminal populations and could be relevant to understanding the significant increase in violence-related mortality observed among people assigned to cholesterol-lowering treatment in clinical trials."(78)
A research monkey after discovering he was going to be placed on a low-fat diet for almost 2 years.
Fatless Shrugged
It was Ayn Rand who once said that the most noble and productive goal for a person to engage in was the pursuit of their own happiness. If the achievement of your own happiness is important to you, then kick the low-fat diet's sad, sorry, melancholy butt right out of your life--it's a loser.
Low-Fat Diets Lower Testosterone
Testosterone is abhorred by politically correct weenies, who like to blame it for every instance of disagreeable male behavior, in much the same way menstruation was once cited as the catch-all explanation for uncharacteristically aggressive or irritable female behavior.
Of course, scientific reality is of little concern to the politically correct. The fact is, testosterone is an extremely important hormone for both men and women. Sex drive, muscle and bone health, immune function, cognitive function, mood, and cardiovascular health are all negatively affected by declining levels of testosterone. Testosterone levels typically decline with age, and, along with the decline of other key hormones, falling T levels are believed to be a major contributor to many of the deleterious changes seen during the aging process. As such, aging individuals should be looking at ways to preserve and even boost their testosterone status, rather than engaging in self-defeating habits that will speed the decline in T levels. Alcohol abuse, recreational drug use, pharmaceutical drugs, stress, and poor sleep habits can all lower testosterone levels.
So too can low-fat diets.
Research shows that reducing fat intake from around forty percent to 20-25 percent of calories decreases testosterone output. Low fat diets also increase levels of sex hormone-binding globulin (SHBG), a protein which binds to testosterone, thus reducing the amount of bioavailable, or 'free', testosterone in the body. It is free testosterone that is responsible for this hormone's favorable effects on growth, repair, sexual capacity and immune function(79-81).
Again, not just any old fat will suffice when it comes to optimizing testosterone levels. A study with weight-training men showed higher saturated fat and monounsaturated fat consumption to be positively associated with testosterone levels. In contrast, higher dietary levels of so-called "heart-healthy" polyunsaturated fats relative to saturated fats were associated with lower testosterone levels (82).
It's highly ironic that athletes and bodybuilders will take all manner of expensive, esoteric and often dubious testosterone-boosting concoctions--not to mention anabolic steroids--yet will follow hormone-damping low-fat diets with religious fervor. It's a little like putting on a weighted vest before a big race and expecting to run at full speed.
Hormones like testosterone play a fundamentally important role in stimulating and regulating growth and metabolism. Don't go throwing a low-fat monkey wrench into your metabolic engine!
Low-Fat Diets and Immune Function
Diet 'experts' assure us that a low-fat diet is the key to good health. The published research does not support such claims.
Despite the virulent ranting of anti-fat activists, trials comparing sedentary adult volunteers fed low-fat diets with those receiving higher fat diets has shown no improvement in immune status in the former group(83,84).
In children, whole milk consumption is associated with fewer gastrointestinal infections than consumption of low fat milk (85). Rats consuming diets high in milk fat show a significantly greater resistance to Listeria infection and higher survival rates than those whose diets were low in milk fat(86). Similar results have been observed in mice fed diets high in saturate-rich coconut oil(87)
In athletes, who are constantly pushing their immune systems to the edge with strenuous training, adherence to the commonly-recommended low-fat high-carbohydrate diet (15-19% of total calories) increases pro-inflammatory immune factors, decreases anti-inflammatory factors, and depresses antioxidant status when compared to higher fat diets (30-50% of total calories)(88,89). Such changes may leave athletes on low-fat diets with a lowered resistance to infection and a higher risk of chronic illness. This may be due to difficulty in obtaining sufficient calories from low-fat diets to meet the energy demands of exercise; increasing dietary fat intake and total caloric intake to match energy expenditure appears to reverse the negative effects on immune function reported on calorie-deficient, low-fat diets. Diets comprising 32% to 55% fat also improve endurance capacity compared to diets with 15% fat(90).
It was Scandinavian researchers who, in the 1960s, performed research showing that using extremely high-carbohydrate, low-fat diets for short periods could enhance athletic performance. This was achieved by using these diets as part of a "depletion-repletion" carbohydrate-loading strategy, which helped temporarily elevate muscle glycogen stores to higher than usual levels. One of the pioneers in this area, Dr. Jan Karlsson, points out that such diets were never intended to be applied for more than 3-4 days. Karlsson and his colleagues openly lament that these diets are now employed for extended periods of time, and refer to the prolonged use of very high-carbohydrate/low-fat diets by athletes as "voluntary malnourishment". They note that in Scandinavia, researchers use the term "Carbohydrate Trap" when referring to the widespread belief that these diets are required for optimal performance. These researchers consider a 50-55% carbohydrate, 35% fat diet to be eminently more sensible and nutritious than the >60% carb, <25% fat diets commonly used by athletes(91).
For athletes and non-athletes alike, the low-fat diet is a sick (pun intended) joke.
The Low-Fat Diet Does Not Protect Against Heart Disease, and May Actually Worsen It
The WHI trial confirmed what well-read cholesterol skeptics have known for a long time: The low-fat diet is a big fat fraud when it comes to preventing heart disease. Among the 48,835 women participating in the trial, no significant differences in CHD or stroke incidence, CHD or stroke mortality, or total mortality were observed(92). Nor were there any reductions in the incidence or mortality rates of breast cancer, colorectal cancer, or total cancer(93,94).
There was however, one very ominous finding to emerge from the WHI trial. Among the 3.4 percent of trial participants with pre-existing cardiovascular disease, those randomized to the low-fat diet experienced a 26% increase in the relative risk of non-fatal and fatal CHD!
Low-fat advocates have remained deafeningly silent on this inconvenient finding, and would no doubt like to believe this was just a 'freak' occurrence. However, this is hardly the first time that low-fat eating has been shown to worsen the prognosis of women with existing cardiovascular disease.
In 2004, the world's most prominent nutrition journal, The American Journal of Clinical Nutrition, published the results of a very, very interesting study. Harvard researchers had taken 235 postmenopausal women with established coronary heart disease, and divided them into four categories according to their level of saturated fat intake. They then performed coronary angiographies at baseline and after a mean follow-up of 3.1 years, analyzing over 2,200 coronary artery segments in the process.
After adjusting for multiple confounders, a higher saturated fat intake was associated with less narrowing of the arteries and less progression of coronary atherosclerosis. Compared with a 0.22 mm narrowing in the lowest quartile of intake, there was a 0.10-mm narrowing in the second quartile, a 0.07 mm narrowing in the third quartile, and no narrowing in the fourth and highest quartile of saturated fat intake!
Following a low-fat diet means adopting a high-carbohydrate diet by default. After all, it is exceedingly difficult and highly unpalatable to achieve the bulk of one's caloric needs by eating lean protein foods. It is of no small concern then, that carbohydrate intake was positively associated with atherosclerotic progression, particularly when the glycemic index was high. The intake of so-called 'heart-healthy' polyunsaturated fats was also positively associated with progression of atherosclerosis, but monounsaturated and total fat intakes were not associated with progression (it must be noted that the major sources of polyunsaturates in Western countries are refined vegetable oils which are rich in the omega-6 fat linoleic acid. The polyunsaturated omega-3 fats, which are underconsumed by most Westerners, have actually been shown to lower CVD).
After examining the baseline data for the study subjects, it is apparent that the results can not be explained away by otherwise healthier lifestyles among those eating the most saturated fat; the high saturated fat group, in fact, had the greatest number of current smokers! Women eating the most saturated fat were also less likely to take blood-thinning medications like aspirin(95).
If this study had found saturated fats to be associated with cardiovascular disease, its results would have been trumpeted in headlines around the world. Instead, they were largely ignored by the mainstream media and our ever-so responsible 'health' authorities. It appears only studies that support the cherished dogma of our health orthodoxy are considered suitable as press release fodder…
A major factor in the progression of cardiovascular disease--and most major diseases--is free radical damage. It is well-established that saturated fatty acids, because of their lack of vulnerable double bonds, are the least susceptible to free radical damage; polyunsaturates are the most vulnerable. We also know that increased carbohydrate consumption, especially of the refined variety, does an outstanding job of raising blood sugar and insulin levels, which accelerates glycation, free radical activity, blood clot formation, and arterial smooth muscle cell proliferation.
It should also be noted that increasing heart disease incidence throughout the twentieth century has been accompanied by increasing polyunsaturate consumption, while a marked increase in refined carbohydrate consumption during the last three decades has been accompanied by spiralling obesity and diabetes incidence. Animal fat consumption, in contrast, has remained stable over the last 100 years.
So what we have is two studies that show that women with pre-existing heart disease will experience WORSE outcomes if they shun saturated fat and opt for a low-fat/high-carbohydrate diet! Furthermore, the validity of these results is supported by basic biochemistry and epidemiological data. So will low-fat advocates stop recommending this pattern of eating to women with heart disease? Does their concern for human life override their need to defend their precious low-fat dogma at all costs?
I truly doubt it…
If low-fat advocates won't be straight with you, then I will. Let's be perfectly clear on this: If you are female, and suffer cardiovascular disease, the published, peer-reviewed scientific evidence indicates that adopting a low-fat diet could be DEADLY.
The WHI is not the only dietary intervention trial to demonstrate the worthlessness of the low-fat diet in preventing CVD. In 1965, the prominent journal Lancet published the results of a trial conducted by the UK Medical Research Committee. In this study, 264 men under 65 were assigned to either a low-fat diet or their usual diet. Dietary records show that those in the low-fat group averaged 45 g/day of fat throughout the trial, while those in the control group actually increased their average fat intake from 106 to 125g. The average serum cholesterol measurement of the low-fat group was 25 points lower than that of the control group at 4 years. Despite nonsensical claims that "every 1mg/dl drop in cholesterol equals a 2% drop in CHD risk", there were no differences between the two groups in CHD incidence or mortality after 4 years.
In Search of the Elusive 'Negative Fat Intake'!
The hysterical anti-fat vitriole that spews forth from some anti-fat faddists leads me to believe that if these clowns could eat a 'negative-fat' diet, they would! As for their argument that the above trials didn't lower fat enough, one has to wonder how creating even greater deficiencies in valuable nutrients, and predisposing one to greater risk of depression and anger--all of which low-fat diets have indeed been clinically documented to do--will in any way help prevent heart disease! Maybe these folks have been eating low-fat so long that it's started to drain their brains; healthy human brains, after all, are 60% fat by weight!
The authors of the MRC trial concluded that: "A low-fat diet has no place in the treatment of myocardial infarction." Despite being written over forty years ago, these words have largely been ignored by a medical and health hierarchy which seems to earnestly believe that if only it keeps flogging the dead low-fat horse, it will one-day magically spring to life. In Australia, this is known as engaging in a 'wank', which means that people who push low-fat diets despite no proof whatsoever of their efficacy are wankers. This might be stating the obvious, but…you really shouldn't listen to wankers!
But the Japanese Eat a Low-Fat Diet…Don't They?
Supporters of low-fat nutrition cite the Japanese ad nauseum, claiming that their low-fat/high-carbohydrate diet is the reason for their low rate of heart disease. It is ironic that many of these same commentators exhort the benefits of whole-grains and tell us that the only 'bad' carbohydrates are those that come from refined sugars and grains. These folks need to get their story straight---a major source of carbohydrates in the Japanese diet is white rice--a refined grain! That means that if the high-carbohydrate Japanese diet is cardio-protective, then refined grains must be good for one's heart! Well, which is it? You can't have it both ways; either refined grains are heart-friendly, or they're not!
The truth is, the longevity and low CHD incidence of the Japanese owes nothing to carbohydrate intake, refined or otherwise. During the 1960s and 1970s, industrialization underwent rapid growth in Japan. This period of marked economic change bought with it greater consumption of animal protein and fat. This increased animal food consumption in Japan has been accompanied by a marked decline in both the overall incidence of and the mortality from one of that nation's biggest killers--stroke. This increase in animal protein and animal fat consumption has also occurred alongside Japan's rise to the top of the longevity ladder.(96,97)
If you're tempted to write this off as merely a consequence of improved living standards and medical technology, keep in mind that long-term follow-up studies with both native and migrant Japanese populations show that those who eat the most animal protein and animal fat enjoy greater longevity and a lower incidence of stroke than those who eat lesser amounts(98-101).
OK, So What About the Mediterranean Diet?
A diet low in saturated fat is purportedly a major factor in the low rates of CHD observed in Southern European countries. Just one wee problem: France, the Mediterranean country with the lowest CHD rates of all, is also the Mediterranean country with the highest saturated fat intake!
Oops!
Health 'experts' have tried to brush off this embarrassing observation as a 'paradox' (orthodoxy loves applying the 'paradox' label to uncomfortable contradictions) by claiming that red wine explains this difference. If that were true, then the Italians, who drink a similar amount of red wine, should have CHD rates even lower than France. But they don't; their CHD rates are similar to those of other Southern European countries where far less red wine is consumed(102).
Conclusion
I could go on, and on, and on…but I'll just close by saying that the low-fat diet has NEVER been demonstrated to do all the wonderful health-fortifying things claimed for it. The only trials showing favorable effects in people following low-fat diets are those that simultaneously employed other truly useful interventions, like exercise, stress management, increased fruit and vegetable intake and decreased processed food intake, and weight loss. However, there is absolutely no law whatsoever stating that low-fat eating is required for the implementation of any of these strategies. In fact, given the available evidence, one can only conclude that the inclusion of higher fat intakes in these trials may even have improved the results!
The bottom line: Not only is low-fat eating a boring way to go through life, it is a useless and often counterproductive hoax.
References and Assorted Disclaimers:
DISGRUNTLED WORSHIPPERS OF THE LOW-FAT RELIGION SHOULD READ THE FOLLOWING:I have not stated anything in this article that cannot be verified by published, peer-reviewed research. Nonetheless, my inbox will no doubt be flooded with angry emails from those who have been brainwashed by the low-fat paradigm, and who violently object to the thought that something that they have believed in so strongly for so long might actually be false. In other words, malevolent dimwits who want to shoot the messenger! For those of you who fall into this category, my suggestions are as follows: 1) GROW UP!; 2) Start placing a premium on discovering the facts, as opposed to doggedly defending what you have already decided you want to believe; 3) Instead of attacking me, start questioning the motives of those who profit greatly from the fallacious anti-fat, anti-cholesterol paradigm. This includes the food and drug conglomerates that make BILLIONS from the sale of low-fat foods and cholesterol-lowering drugs, the health and dietetic 'associations/organizations/institutes/foundations/etc' who receive millions in 'donations' from these very same companies, and the executives of these so-called 'non-profit' organizations who enjoy six-figure incomes and extensive perquisites.
To attack the owner of a non-commercial web site, who has nothing to gain financially by either supporting or opposing the low-fat paradigm, while defending those WHO DO, is so bloody stupid that it defies comprehension. Unfortunately, there are a lot of bloody stupid people in the world! If you are one of them, and decide to write me, please note that unless your email contains valid references to the scientific literature, it will be deleted immediately. After having established yourself as an ignorant goofball, your email address will also be added to my spam filter and any further emails will be delivered straight to my trash. Sorry, but I really am extremely busy and have no time or patience for ignorant, time-wasting twits.
NOTE: I have no problem with people reprinting this article on other web sites for non-commercial purposes. Heck, you can post it on the side of the Empire State Building for all I care (just be sure to seek permission from the owners first)! However, PLEASE ENSURE that you give full credit to the author, whether you reproduce the article in whole or part. A hyperlink to www.TheOmnivore.com would also be greatly appreciated! Those wishing to reprint this or any other article on TheOmnivore.com for commercial purposes should email: ac.theomnivore@gmail.com
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95. Mozaffarian D, et al. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. American Journal of Clinical Nutrition, 2004; 80: 1175-1184.
96. Tanaka H, et al. Secular trends in mortality for cerebrovascular disease in Japan, 1960-1979. Stroke, 1982; 13: 574-581.
97. Nakayama C, et al. A 15.5-Year Follow-up Study of Stroke in a Japanese Provincial City: The Shibata Study. Stroke, Jan 1, 1997; 28(1): 45-52.
98. Iso H, et al. Fat and protein intakes and risk of intraparenchymal hemorrhage among middle-aged Japanese. American Journal of Epidemiology, Jan 1, 2003; 157 (1): 32-39.
99. Abbott RD, et al. Effect of dietary calcium and milk consumption on risk of thromboembolic stroke in older middle-aged men: The Honolulu Heart Program. Stroke, May 1996; 27: 813 - 818.
100. Sauvaget C, et al. Intake of animal products and stroke mortality in the Hiroshima/Nagasaki Life Span Study. International Journal of Epidemiology, Aug 1, 2003; 32 (4): 536-543.
101. Sauvaget C, et al. Animal Protein, Animal Fat, and Cholesterol Intakes and Risk of Cerebral Infarction Mortality in the Adult Health Study. Stroke, 2004; 35: 1531.
102. Food intake data from Food and Agriculture Organization of the United Nations, Statistical Database. CHD mortality data from World Health Statistics Annual, 1961, 1966 and 1997-1999 editions.
What to Do About Inconvenient Facts?
"The great tragedy of Science -- the slaying of a beautiful hypothesis by an ugly fact."
-- Thomas Huxley
So begins an article today in TSC Daily, Eating Some Crow on Fat, by John Luik.
The attitude of we-know-best-no-matter-what-the-studies-say discredits both the scientific process and the requirement that health advice be evidence-based. It risks turning off a population already weary and wary of the lifestyle solutions offered up by the medical community. And it ignores a fundamental responsibility that attaches to providing risk advice: If the science changes, amend your advice. To do otherwise changes the enterprise from advice-giving to propaganda-making. However beautiful the hypothesis, the "ugly" facts are always preferable.
It's one of those articles you have to read - no need for analysis from me!
-- Thomas Huxley
So begins an article today in TSC Daily, Eating Some Crow on Fat, by John Luik.
The attitude of we-know-best-no-matter-what-the-studies-say discredits both the scientific process and the requirement that health advice be evidence-based. It risks turning off a population already weary and wary of the lifestyle solutions offered up by the medical community. And it ignores a fundamental responsibility that attaches to providing risk advice: If the science changes, amend your advice. To do otherwise changes the enterprise from advice-giving to propaganda-making. However beautiful the hypothesis, the "ugly" facts are always preferable.
It's one of those articles you have to read - no need for analysis from me!
Thursday, February 23, 2006
From the Fat Files
It's amusing to read all the excuses advanced to dismiss the null findings from the WHI Dietary Modification Trial - my favorite is the one that claims that reducing fat is passe, that we'd moved on from that thinking about the time the study was just getting underway.
We find this excuse in a number of articles, but a quote in the International Herald Tribune in their article, Chances a low-fat diet will help? Slim and none, really is the best - "The diets studied "had an antique patina," said Dr. Peter Libby, a cardiologist and professor at Harvard Medical School. These days, Libby said, most people have moved on from the idea of controlling total fat to the idea that people should eat different kinds of fat."
Oh really? Then why are the studies still being published in the medical journals so focused on total fat?
Yesterday I wrote about a study published in November 2005, last week, a study published this month, and today, let's take a look at one published in April 2004 - Effect of low and high fat diets on nutrient intakes and selected cardiovascular risk factors in sedentary men and women.
This one placed study subjects on two different diets - one that was just 19% fat and another than was an eye-popping 50% fat. Guess who did better? If you said those on the low-fat diet, you're wrong. Those on the 50% fat diet increased their HDL-C to an amazing 63! The researchers noted that those on the low-fat diet may not be able to consume ENOUGH calories on such a diet, that the low-fat diet was deficient in essential fatty acids, missed essential micronutrients (especially zinc and Vitamin E) and also lowered ApoA1.
Guess the media missed that one too, huh?
Amazing when you think about it - the media only seems to find and provide information about studies that support the low-fat paradigm - and even when they do include one that clearly shows no benefit, they advance the message that something was wrong with the study - be it not enough time or those in the study just didn't lower their fat enough!
How about another example that illustrates how diet can affect risk markers? Back in May 2003, the Tohoku Journal of Experimental Medicine published the findings of a study on diabetic patients - Effects of diet treatment on some biochemical and physiological parameters in patients with type 2 diabetes mellitus. The conclusions offer no real insight to what happened to those with diabetes: This study showed that diet treatment could not normalize the high systolic blood pressure in type 2 DM. Thus, an effective way of controlling blood pressure should be taken to improve healing in DM.
Want to know what really happened? Well, when they had their diet changed to 50-55% carbohydrate, 30% fat and 15-20% protein....heck I'm not afraid to tell you...
We find this excuse in a number of articles, but a quote in the International Herald Tribune in their article, Chances a low-fat diet will help? Slim and none, really is the best - "The diets studied "had an antique patina," said Dr. Peter Libby, a cardiologist and professor at Harvard Medical School. These days, Libby said, most people have moved on from the idea of controlling total fat to the idea that people should eat different kinds of fat."
Oh really? Then why are the studies still being published in the medical journals so focused on total fat?
Yesterday I wrote about a study published in November 2005, last week, a study published this month, and today, let's take a look at one published in April 2004 - Effect of low and high fat diets on nutrient intakes and selected cardiovascular risk factors in sedentary men and women.
This one placed study subjects on two different diets - one that was just 19% fat and another than was an eye-popping 50% fat. Guess who did better? If you said those on the low-fat diet, you're wrong. Those on the 50% fat diet increased their HDL-C to an amazing 63! The researchers noted that those on the low-fat diet may not be able to consume ENOUGH calories on such a diet, that the low-fat diet was deficient in essential fatty acids, missed essential micronutrients (especially zinc and Vitamin E) and also lowered ApoA1.
Guess the media missed that one too, huh?
Amazing when you think about it - the media only seems to find and provide information about studies that support the low-fat paradigm - and even when they do include one that clearly shows no benefit, they advance the message that something was wrong with the study - be it not enough time or those in the study just didn't lower their fat enough!
How about another example that illustrates how diet can affect risk markers? Back in May 2003, the Tohoku Journal of Experimental Medicine published the findings of a study on diabetic patients - Effects of diet treatment on some biochemical and physiological parameters in patients with type 2 diabetes mellitus. The conclusions offer no real insight to what happened to those with diabetes: This study showed that diet treatment could not normalize the high systolic blood pressure in type 2 DM. Thus, an effective way of controlling blood pressure should be taken to improve healing in DM.
Want to know what really happened? Well, when they had their diet changed to 50-55% carbohydrate, 30% fat and 15-20% protein....heck I'm not afraid to tell you...
- Total Cholesterol - decreased from 231 to 227
- LDL - INCREASED from 139.4 to 150.9
- HDL - DECREASED from 44.4 to 40.2
- Triglycerides decreased from 290 to 192.4
- TC/HDL Ratio - INCREASED from 5.2 to 5.64 (an increase is BAD)
- Blood pressure - INCREASED from 114/87 to 139/85
Yet the best the researchers could conclude in their abstract was that the diet couldn't normalize systolic blood pressure? Good grief - the diet intervention made these folks worse! Here though, the researchers did at least have the guts to state "Increasing fat intake to 50% of calories improved nutritional status, and did not negatively affect certain cardiovascular risk factors," in the full-text portion of their paper.
Not a peep from the media though.
Not a word of caution to diabetics from the American Diabetes Association either.
Not even the review, published in the American Journal of Cardiology - High-density lipoprotein as a therapeutic target: clinical evidence and treatment strategies - received the attention it should have.
In it, the authors state, quite clearly, "The clinical importance of low serum levels of high-density lipoprotein (HDL) cholesterol is often under-recognized and underappreciated as a risk factor for premature atherosclerosis as well as for cardiovascular morbidity and mortality. Low serum levels of HDL are frequently encountered, especially in patients who are obese or have the metabolic syndrome. In prospective epidemiologic studies, every 1-mg/dL increase in HDL is associated with a 2% to 3% decrease in coronary artery disease risk, independent of low-density lipoprotein (LDL) cholesterol and triglyceride (TG) levels."
Yet we continue to see the media and experts hone in our lowering of total cholesterol and LDL as beneficial even when the cited studies show a decrease in HDL and worse TC/HDL ratios! Folks, that's NOT a benefit for long-term health.
If you haven't started to notice, there are a number of studies out there that show we're still looking in all the wrong places (trying to lower total fat intake) and that the contention that we're long past that is way off base. We're entrenched in it and still fail to appreciate how dietary fats - yes even the much maligned saturated fats - increase HDL while reducing the TC/HDL ratio, which is considered a good number to use to predict cardiovascular disease!
Wednesday, February 22, 2006
What Does Saturated Fat Do to Your Cholesterol?
The American Heart Association continues to advance the belief that saturated fat is bad for our hearts, and specifically recommends that we do our best to achieve a "desirable choleserol level" by a variety of dietary changes, including:
- Limit foods with a high content of saturated fat and cholesterol. Substitute with grains and unsaturated fat from vegetables, fish, legumes and nuts.
- Limit cholesterol to 300 milligrams (mg) a day for the general population, and 200 mg a day for those with heart disease or its risk factors.
- Include fat-free and low-fat dairy products, fish, legumes, poultry and lean meats.
A study was published last year in the American Journal of Clinical Nutrition (November 2005) that followed a group of 86-men, aged 22-64 eating three different diets. Meals were prepared for them to maintain compliance with the dietary changes and the fat content of each diet was manipulated by using different dairy products - full-fat, reduced fat and non-fat.
The results are quite telling about how saturated fats and our intake of dietary cholesterol affect our cholesterol.
Before we look at the findings, let's see what the diets looked like:
The "Average American Diet" (ADD)
- 36.8% fat (14% SFA, 14.5% MUFA, 8.3% PUFA)
- 49.6% carbohydrate
- 13.6% protein
- 104mg cholesterol/1000 calories
The "Step I Diet"
- 28.1% fat (8.8% SFA, 11.5% MUFA, 7.9% PUFA)
- 58% carbohydrate
- 13.9% protein
- 76mg cholesterol/1000 calories
The "Step II Diet"
- 23.7% fat (6.2% SFA, 9.7% MUFA, 7.8% PUFA)
- 61.9% carbohydrate
- 14.4% protein
- 63mg cholesterol/1000 calories
All participants were fed an isocaloric diet to maintain their weight and the calorie levels ranged from 2200-3400 since each participant ate what they needed to maintain their weight. If their weight fluctuated more than 1kg, their diet was adjusted until their weight returned to their intial weight. This is an important factor in this study - the men were neither allowed to gain or lose weight during the intervention periods. What this allows is a clean look at how dietary fat is impacting various measures of health without the confounding variable of weight change.
At baseline, the men had an average
- Total Cholesterol = 186.34
- LDL Cholesterol = 126.41
- HDL Cholesterol = 40.20
- Triglycerides = 96.57
- TC/HDL Ratio = 4.63
And, let's be clear - these guys were pretty average...the average BMI was 25.6 (range was 22-33.2)
Wonder what each diet did to their cholesterol levels? Well, you might be surprised....
The Step II Diet (the one you might think was the healthiest) did the worst, even though it effectively lowered total cholesterol the most, from 186.34 to 169.71. LDL was reduced from 126.41 to 110.95, but HDL was also reduced from 40.20 to 36.72 and triglycerides rose from 96.57 to 108.09.
The Step I Diet fared slightly better, but still wasn't an improvement when we take a close look. Total cholesterol declined from 186.34 to 177.44 with LDL decreasing from 126.41 to 117.13 - but again, the diet also took it's toll on HDL, causing it to decrease from 40.20 to 38.27. Triglycerides also rose from 96.57 to 106.32.
The real surprise was that the ADD diet actually made some improvements in cholesterol. Total cholesterol remained 186.34, but LDL declined slightly to 125.64 and HDL rose from 40.20 to 41.36, while triglycerides declined from 96.57 to 93.91.
The researchers did a number of analysis - in the hope to find some redeeming value for the low-fat diets - to no avail. No matter how hard they looked, no matter what parameter they analyzed (from BMI to glucose, from insulin to waist circumferance, from body fat percentage to HOMA score) the lower fat diets performed poorly.
You wouldn't know that from the abstract though - in it the researchers merely conclude "Persons who are insulin resistant respond less favorably to Step II diets than do those who are insulin sensitive."
Noteworthy in the full-text of the paper is this observation from the researchers - "Being overweight and the associated insulin resistance that can lead to the metabolic syndrome is a growing health problem. Only 7% of our study population met the criteria for having metabolic syndrome as defined by National Cholesterol Education Program. Nonetheless, the participants who were overweight or who had higher insulin concentrations had altered metabolic responses to lower fat diets. Thus, the effects of elevated insulin concentrations on the LDL-cholesterol and triacylglycerol responses preceded the development of overt metabolic syndrome."
It's estimated that 25% of Americans already are affected by the features of Metabolic Syndrome - this particular study only had 7% within its subjects, and yet - even before they met the criteria for Metabolic Syndrome - if they were overweight and had higher insulin concentrations, the Step I and Step II Diets were bad news for their cholesterol!
If you recall, this was published in November 2005 - just three months ago. This month we had the Women's Health Initiative Dietary Modification Trial show that low-fat diets did not improve cholesterol or reduce the risk of breast cancer, colon cancer or cardiovascular disease. There are many other studies out there too that have resulted in similar findings. Yet, the AHA and others continue to march to the beat of dogma instead of evidence-based standards.
In an editorial regarding this study, the author, Jose Ordovas, notes this when he wrote "These results were, on average, similar to those from many previous studies that used similar experimental designs and diets."
Ordovas continues later with "The other relevant outcome of the study relates to the results obtained for the ratio of total to HDL cholesterol, also known as the atherogenic ratio. Higher values have been associated with an increased CVD risk. Therefore, the elevations observed after the Step I and II diets cast some concerns about the efficacy of these low-fat diets to reduce CVD risk."
He then quickly retreats however, and instead looks to call the study design into question "However, experimental design may have been the driving force for the increased ratio of total to HDL cholesterol and triacylglycerol concentrations observed after the low-fat diets," even though he'd previously praised the design earlier "Lefevre et al's study design fulfills many of the expectations of a well-conducted dietary intervention study, namely, a randomized, double-blind, 3-period crossover controlled feeding design. In addition, these investigators take multiple measurements per dietary phase, which reduces the confounding of intraindividual variability. Moreover, they chemically measured the menus provided, thereby connecting the calculated with the actual composition of the diets."
He ends by saying that "the first baby steps can be seen already in the most current version of the US Department of Agriculture pyramid (www.mypyramid.gov). Perhaps at some time in the future, the current controversies will be put to rest. We will be able to identify those persons for whom diet plays no major role in their risk of CVD and this should appease those who defend the diet-heart null hypothesis. The same tools will identify those persons who may benefit more from one of the many potentially beneficial diets currently proposed."
This leads a reader to believe that someone in the study, on the Step I or Step II Diets, actually saw an improvement in their cholesterol! There is no data to suggest such a leap of faith.
Basically, he tows the line and maintains the message that the Dietary Guidelines for Americans (DGA), which is close to the Step I Diet, is just fine and dandy.
This study, taken with the number of other studies that have reached similar findings should be reason enough to demand we cease-and-desist with these guidelines. With 25% of the adult population already presenting features of Metabolic Syndrome, such dietary recommendations will continue to exacerbate the problem, not make things better.
Folks, just look at the data for yourself - reducing your saturated fats and using "good" monounsaturated and polyunsaturated instead, even lowering your total fat - does nothing to improve your cholesterol! Using low-fat and fat-free dairy in place of whole milk dairy - that too does nothing to improve your cholesterol! Lowering your intake of dietary cholesterol - yup, that too does nothing to improve your cholesterol. But you wouldn't know that if you listen to the "experts" and don't read the data for yourself, would you?
Tuesday, February 21, 2006
Low-Carb - High-Carb - Protein...What Does the Data Tell Us?
One of the largest meta-regressions to review the effects of low-to-moderate carbohydrate diets was published this month in the American Journal of Clinical Nutrition, Effects of variation in protein and carbohydrate intake on body mass and composition during energy restriction: a meta-regression. This particular review has received no mention in the press - most likely because the null findings from the WHI Dietary Modification Trial continues to dominate the headlines.
It's an important review however, bringing together a comprehensive and impressive set of data - 87 studies made the cut and were included in the analysis. Oh, and I think it's important to note, the researchers in this study - from the Department of Food Science and Human Nutrition and of Statistics, University of Florida - none have previously published studies investigating low-carb diets or low-fat diets. Noteable too is the conflict-of-interest disclosure - the paper was not the product of any outside funding - in fact, the paper states the lead researcher, James W Krieger, funded the effort.
So, then, let's get to the good stuff - what the researchers wanted to know and what they found when they started looking at all this data! They reviewed a number of factors:
It's an important review however, bringing together a comprehensive and impressive set of data - 87 studies made the cut and were included in the analysis. Oh, and I think it's important to note, the researchers in this study - from the Department of Food Science and Human Nutrition and of Statistics, University of Florida - none have previously published studies investigating low-carb diets or low-fat diets. Noteable too is the conflict-of-interest disclosure - the paper was not the product of any outside funding - in fact, the paper states the lead researcher, James W Krieger, funded the effort.
So, then, let's get to the good stuff - what the researchers wanted to know and what they found when they started looking at all this data! They reviewed a number of factors:
- Body mass change
- Fat-free mass change
- Percentage changes in body fat
- Fat mass changes
After this comprehensive review and analysis, their conclusion was "Low-carbohydrate, high-protein diets favorably affect body mass and composition independent of energy intake, which in part supports the proposed metabolic advantage of these diets."
Body mass change
Diets with carbohydrate intake in the lowest quartile were associated with a 1.6–1.7kg greater body-mass loss than were diets with carbohydrate intake in the highest 3 quartiles. When carbohydrate intake was categorized as low or high, the significant effect in the low-carbohydrate intake group remained.
Fat-free mass (FFM) change
The amount of FFM retained tended to increase with each successive quartile of protein intake, with a significant difference existing between the upper 2 quartiles (greater than 1.05g/kg) and the first quartile (0.7g/kg). Specifically, the third quartile ( greater than 1.05 and 1.2g/kg) was associated with 0.78kg additional FFM retention and the fourth quartile (greater than 1.2g/kg) was associated with 0.96kg additional FFM retention.
Compared with carbohydrate intake in the lowest quartile, the carbohydrate intake in the highest quartile was associated with 0.98kg greater FFM retention. Carbohydrate intake in the second and third quartiles tended to be associated with 0.62–0.65kg more FFM retention.
In their discussion, the researchers state "Protein intake was a significant predictor of FFM retention. A daily protein intake of greater than 1.05g/kg was associated with a greater FFM retention than was a protein intake closer to the RDA. The magnitude of this effect increased when studies of greater than 3-mo duration were analyzed. Thus, the protein RDA may not be optimal for FFM retention during energy restriction, particularly during prolonged periods of dieting. Energy restriction can decrease nitrogen balance and thus decrease the amount of protein and FFM retained by the body. An increase in protein intake would increase nitrogen balance and thus increase the amount of FFM retained."
Percentage changes in body fat (BF)
Diets with a carbohydrate intake in the lowest quartile were associated with a 1.32–1.48% greater decrease in percentage BF than were diets with carbohydrate intake in the highest 3 quartiles. When carbohydrate intake was categorized as low or high, the significantly greater decrease in percentage BF in the low-carbohydrate intake group remained.
Fat mass (FM) changes
Diets with carbohydrate intake in the lowest quartile were associated with a 1.79–2.32kg greater loss of FM than were diets with carbohydrate intake in the highest 3 quartiles. When carbohydrate intake was categorized as low or high, low-carbohydrate diets were associated with a greater loss of FM than were high-carbohydrate diets.
One claim often made by those who insist that low-carb diets are not effective is the contention that weight loss is just water loss. Here, the researchers are clear - "Compared with higher carbohydrate intakes, low-carbohydrate diets increased the loss of body mass, BF, and percentage BF, even after control for energy intake as a covariate in the regression analyses. The mean total carbohydrate intake in the low-carbohydrate studies ranged from 79g–97g, depending on the analysis. Typically, a carbohydrate intake of less than 100g will cause ketosis. These results support the apparent metabolic advantage of low-carbohydrate, ketogenic diets. The additional body mass change is not likely due to water loss, because the duration of the diet periods (6–24 wk) was too protracted and estimations of total body water tend to be similar between low-carbohydrate and low-fat diets after 2-wk. The similar results of the analyses on body mass and BF also supports the concept that the effect on body mass of low-carbohydrate diets is an effect on FM rather than on body water."
At the end of their discussion, the researchers - a second time - make a bold statement - In conclusion, low-carbohydrate diets may increase the loss of body mass, FFM, FM, and percentage BF during weight reduction compared with traditional diets. The RDA for protein may be insufficient for optimal FFM retention during weight loss; high protein intakes (greater than 1.05g/kg) may improve FFM retention.
The researchers did a good job of selecting studies and weeding out those that did not meet their inclusion criteria. If you recall, last week I wrote about how poor data results in useless analysis in my article Comparing Low-Carb to Low-Fat: Analyzing a review. A quality review requires quality data - quality data comes from participants actually sticking with a particular dietary approach.
More importantly, this particular review highlights the importance of protein intake. The researchers took the additional step to analyze not percentage of calories, but actual gram intake in each study. This approach allowed us to gain a better understanding of how critical protein is in our diet. Those consuming protein at the RDA did much worse than those consuming a higher protein intake.
The review puts the spotlight on just how important protein consumption is when you're following a weight loss diet - higher in carbohydrate or lower in carbohydrate - protein is a critical, essential nutrient and if you reduce your intake of protein, you'll lose more lean body mass. This fact is all the more obvious in this review and calls into question, once again, the standard recommendation to consume protein as a percentage of calories (10-15%) while trying to lose weight. As I've pointed out a number of times - following that advice reduces protein intake dramatically - something this paper clearly shows is detrimental to lean body mass in weight loss regardless of carbohydrate intake.
Let's not forget, protein isn't just an essential nutrient - it also offers a higher degree of satiety when one is trying to lose weight too!Take away message from this review - low-carb diets work, they do have a metabolic advantage and it's critical to make sure you're eating enough protein each day while keeping your carbohydrate intake low!
Monday, February 20, 2006
In the Thin - Why Calories May Not Matter
In the article, Study: Watching Calories Takes Commitment, there's no mention of the various letters challenging the study findings as they relate to humans. In fact, a read of the article will leave you with the impression that the author's concluded that calorie restriction will extend your life span. In their published studies, they didn't reach that conclusion - in fact, they reported their findings as relevant to primate species and were careful not to extend their findings to homo sapien.
More troubling though is the Washington Post article statement that "Losing that extra weight is one thing. Keeping it off requires a lifetime of counting calories," followed two sentences later with "Genetic differences allow some primates to remain thin and others to grow fat when fed an identical diet over the years, the study found."
So, which is - did the thin monkeys have to restrict calories or not to remain thin? Apparently not - some grew heavier with an IDENTICAL diet as their thinner counterparts. Somehow that's totally lost in the article and we're told instead that only a lifetime of counting calories is going to keep us slim. On identical calories some grew fatter than others. The researchers chalked that up to genetic differences. The author of the article decided that calorie restriction solves that problem.
What's missing?
Discussion of the metabolic changes that were going on in those monkeys that grew heavier on the same diet - loss of insulin sensitivity, rising blood sugars, rising insulin levels, diabetes. In fact, insulin sensitivity, or lack thereof, was the leading predictor of death in the monkeys. As the study abstract states, "Hyperinsulinemia led to a 3.7-fold increased risk of death (p = less than 0.05);"
That's not specifically genetic - that's a specific metabolic process going awry.
Might genetics play a role in such declines in metabolic function? Absolutely.
Might it be something else, like the burden of long-term diet that may be inappropriate? Absolutely.
Might it be something else, like a combination of factors aligning to create a metabolic nightmare like the Perfect Storm? Absolutely.
We just don't know all the answers at this point in time.
We certainly have clues - and when it comes to humans, we know how deadly high blood sugars, hyperinsulinemia and metabolic syndrome are. Reversing these conditions can be as simple as changing your diet to limit carbohydrate consumption to limit the insulin response to high blood sugars and thus increase insulin sensitivity. Often, the result of carbohydrate restriction is a spontaneous reduction in calorie intake - that is, it happens without effort to restrict calories. That often leads to weight loss, increased insulin sensitivity and overall improvements to risk factors.
Yet, this fairly simple approach is not the standard of care - instead we insist one must eat a low-fat, carbohydrate rich diet to avoid that nasty fat, use an assortment of pharmaceutical interventions to "treat" the symptoms and manage insulin levels, and watch helplessly as the inevitable happens - decline and degradation of the body.
Calorie restriction may alleviate some of the symptoms, but it's not reversing the condition, it's not addressing the root problem - high blood sugars. To fully tackle that issue in the metabolism, only one thing effectively works without drugs - restricting carbohydrate!
More troubling though is the Washington Post article statement that "Losing that extra weight is one thing. Keeping it off requires a lifetime of counting calories," followed two sentences later with "Genetic differences allow some primates to remain thin and others to grow fat when fed an identical diet over the years, the study found."
So, which is - did the thin monkeys have to restrict calories or not to remain thin? Apparently not - some grew heavier with an IDENTICAL diet as their thinner counterparts. Somehow that's totally lost in the article and we're told instead that only a lifetime of counting calories is going to keep us slim. On identical calories some grew fatter than others. The researchers chalked that up to genetic differences. The author of the article decided that calorie restriction solves that problem.
What's missing?
Discussion of the metabolic changes that were going on in those monkeys that grew heavier on the same diet - loss of insulin sensitivity, rising blood sugars, rising insulin levels, diabetes. In fact, insulin sensitivity, or lack thereof, was the leading predictor of death in the monkeys. As the study abstract states, "Hyperinsulinemia led to a 3.7-fold increased risk of death (p = less than 0.05);"
That's not specifically genetic - that's a specific metabolic process going awry.
Might genetics play a role in such declines in metabolic function? Absolutely.
Might it be something else, like the burden of long-term diet that may be inappropriate? Absolutely.
Might it be something else, like a combination of factors aligning to create a metabolic nightmare like the Perfect Storm? Absolutely.
We just don't know all the answers at this point in time.
We certainly have clues - and when it comes to humans, we know how deadly high blood sugars, hyperinsulinemia and metabolic syndrome are. Reversing these conditions can be as simple as changing your diet to limit carbohydrate consumption to limit the insulin response to high blood sugars and thus increase insulin sensitivity. Often, the result of carbohydrate restriction is a spontaneous reduction in calorie intake - that is, it happens without effort to restrict calories. That often leads to weight loss, increased insulin sensitivity and overall improvements to risk factors.
Yet, this fairly simple approach is not the standard of care - instead we insist one must eat a low-fat, carbohydrate rich diet to avoid that nasty fat, use an assortment of pharmaceutical interventions to "treat" the symptoms and manage insulin levels, and watch helplessly as the inevitable happens - decline and degradation of the body.
Calorie restriction may alleviate some of the symptoms, but it's not reversing the condition, it's not addressing the root problem - high blood sugars. To fully tackle that issue in the metabolism, only one thing effectively works without drugs - restricting carbohydrate!
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