You've gotta love it when research findings contrary to the conventional wisdom don't do much to change the status quo or even challenge the assumptions we hold. Take for instance our belief that fruit is important in our diet and must be eaten each day to make sure we're eating a healthy-balanced diet.
True? Probably not.
The data from various studies have shown many times that long-term health is not dependent upon eating fruit, nor any specific quantity of fruit each day. Yet, that hasn't stopped the leading health organizations and government policy makers from repeatedly telling us to eat fruit, warning that diets that limit or restrict fruit are bad, and that we all need at least 2-3 servings a day or we're going to have health problems.
Now don't get me wrong - fruit is good, I like it, I eat it too; but it's just not essential for our long-term health; especially if we're eating a nutrient-rich diet and including non-starchy vegetables.
The latest study to explore the necessity of fruit in the diet was published in the October 24 issue of Neurology - Associations of vegetable and fruit consumption with age-related cognitive change - to investigate the role fuits and vegetables in the diet had for protecting against cognitive decline as we age. Just as the Nurses' Health Study data showed previously, fruit consumption was not associated with a slower rate of cognitive decline, but vegetables, specifically non-starchy vegetables, were protective!
As reported by CBC News - the study "found that high consumption of fruit had no effect on thinking ability."The lead researcher, Dr. Martha Clare Morris, said "By far, the association with a slower rate of decline was found in the group that ate high amounts of green, leafy vegetables." Such foods included lettuce and tossed salad, spinach, kale and collards. The study also found that the slowdown in cognitive decline was greatest in the oldest people who ate at least two more vegetable servings a day.
Take home message here - eat your vegetables, specifically non-starchy vegetables.
So far as fruit - it's fine to include in your diet if you want to, I just don't think you must include fruit to be healthy; it's a nice, sweet addition that also packs in antioxidants; but there doesn't appear to be any big benefit long-term to eating fruit every day.
Interestingly, some countries with better health and longevity actually eat less fruit each day than we do in the United States. So next time you hear about how miserable our intake of fruit is in the US, remember too that Japan, France, Iceland, Switzerland and others eat less fruit than we already do and they live longer and in better health too. Keep in mind they each, also, eat a lot more non-starchy vegetables each day!
Monday, October 30, 2006
Do You Glow in the Dark with Diabetes?
Yahoo! News recently carried a press release about a study published from researchers in the Neatherlands; their finding - subjects with diabetes glow in the dark. The researchers investigated the use of a new non-invasive tool to determine if it could accurately detect skin florescence due to the accumulation of AGEs (advanced glycosylation end products) in the skin of those with diabetes. AGEs are produced in the body when glucose binds with proteins - as they build up, they damage blood vessels and cause complications such as nerve and vascular damage.
From previous studies (Dec 2005; June 2005; July 2004) the researchers knew these AGEs have florescent properties, and this study "confirmed that those properties could be measured by illuminating the skin, and that high levels of autofluorescence were associated with more severe diabetes complications, such as neuropathy, retinopathy and cardiovascular problems."
The lead researcher, Dr. Helen Lutgers, said of the finding, "With this tool, doctors could easily check people with diabetes in an outpatient clinic setting to see whether they may already be developing dangerous complications. The sooner complications are detected, the better the chance of preventing progression of damage."
Here's the rub - while the device used in the study, DiagnOptics AGE-Reader, is available commercially in Europe and is being used by doctors there, it isn't available to healthcare professionals here in the US because it is "restricted to experimental use only," as it awaits FDA approval.
How insane is that? A non-invasive device - shine a light and then in 30-seconds have a result that offers a good measure of accumulated AGEs in the skin by the elbow - that can't get past the FDA approval process?
This is some pretty cool technology if you ask me. It's non-invasive, quick and from the data thus far, reliable and accurate. Considering the very damaging complications from diabetes, especially from AGEs, use of this type of device should be "standard of care" for those with diabetes. I'd even go so far as saying it would be a great add-on in the "standard of care" for any doctor's office visit since the test is quick and simple and the result could prompt further testing to see if someone who has a high measure of florescence has undiagnosed diabetes and is already suffering with complications even though they don't know it!
From previous studies (Dec 2005; June 2005; July 2004) the researchers knew these AGEs have florescent properties, and this study "confirmed that those properties could be measured by illuminating the skin, and that high levels of autofluorescence were associated with more severe diabetes complications, such as neuropathy, retinopathy and cardiovascular problems."
The lead researcher, Dr. Helen Lutgers, said of the finding, "With this tool, doctors could easily check people with diabetes in an outpatient clinic setting to see whether they may already be developing dangerous complications. The sooner complications are detected, the better the chance of preventing progression of damage."
Here's the rub - while the device used in the study, DiagnOptics AGE-Reader, is available commercially in Europe and is being used by doctors there, it isn't available to healthcare professionals here in the US because it is "restricted to experimental use only," as it awaits FDA approval.
How insane is that? A non-invasive device - shine a light and then in 30-seconds have a result that offers a good measure of accumulated AGEs in the skin by the elbow - that can't get past the FDA approval process?
This is some pretty cool technology if you ask me. It's non-invasive, quick and from the data thus far, reliable and accurate. Considering the very damaging complications from diabetes, especially from AGEs, use of this type of device should be "standard of care" for those with diabetes. I'd even go so far as saying it would be a great add-on in the "standard of care" for any doctor's office visit since the test is quick and simple and the result could prompt further testing to see if someone who has a high measure of florescence has undiagnosed diabetes and is already suffering with complications even though they don't know it!
More Moore
Jimmy Moore, the author of Livin' La Vida Low Carb blog and book has hit the airwaves with his own show - the Livin’ La Vida Low-Carb Show. He once weighed over 400 pounds, then lost over 180 of those pounds following a low-carb diet and has never looked back.
The new weekly podcast is hosted by Grasshopper New Media and new episodes are broadcast each Monday. His strongest belief is that the power to change is in your hands and he hopes the podcasts will inspire.
If you're trying to lose weight - how you do it is up to you. His experience is there to help you "Just do it."
Take a moment and drop on over and check out his new show.
The new weekly podcast is hosted by Grasshopper New Media and new episodes are broadcast each Monday. His strongest belief is that the power to change is in your hands and he hopes the podcasts will inspire.
If you're trying to lose weight - how you do it is up to you. His experience is there to help you "Just do it."
Take a moment and drop on over and check out his new show.
Friday, October 27, 2006
Canaries in the Mine
Chalk up another important study the media isn't talking about...The November issue of Diabetes Care published Trends in Hyperinsulinemia Among Nondiabetic Adults in the U.S. which found the mean fasting insulin of non-diabetic adults rose approximately 5% from the NHANES III survey in 1988-1994 to NHANES 1999-2000.
The researchers concluded in the abstract "In parallel with the obesity epidemic, concentrations of fasting insulin and prevalence of hyperinsulinemia have increased remarkably among nondiabetic U.S. adults."
As the researchers noted, focusing on fasting hyperinsulinemia has two advantages:
The researchers concluded in the abstract "In parallel with the obesity epidemic, concentrations of fasting insulin and prevalence of hyperinsulinemia have increased remarkably among nondiabetic U.S. adults."
As the researchers noted, focusing on fasting hyperinsulinemia has two advantages:
- it is as good a surrogate estimate of insulin resistance as are various combinations of fasting insulin and glucose concentration such as homeostasis model assessment or quantitative insulin sensitivity check index.
- of greater clinical relevance is the pathophysiological role that hyperinsulinemia plays in the development of the abnormalities and clinical syndromes that occur more commonly in insulin-resistant subjects. Thus, quantifying the changes in fasting insulin concentration over time provides information regarding both the increasing prevalence of insulin resistance and the potential clinical consequences of this phenomenon.
Put simply - we have a problem in the United States; if it is not reversed it will mean a higher incidence of chronic degenerative disease in our population in years to come.
The researchers provide a laundry list of what hyperinsulemia and insulin resistance is associated with in terms of health outcomes "increased risk of type 2 diabetes, coronary heart disease, essential hypertension, congestive heart failure, polycystic ovarian disease, nonalcoholic fatty liver disease, and cancers of certain sites such as prostate, colon and rectum, and breast.
These chronic diseases are major causes of death in the U.S. and other regions in the world. Furthermore, the burden of these chronic diseases has been growing in the U.S. and worldwide. Rapidly increasing trends in insulin resistance and compensatory hyperinsulinemia, if not properly controlled or altered, may predict adverse future courses of many health conditions that are linked to insulin resistance."
I would have liked to see a more thorough discussion in the full-text about the changes that have occured concurrently with these findings, but the researchers only noted that "[t]he alarming increase in hyperinsulinemia, particularly among groups with a lower prevalence of insulin resistance, such as young adults and non-Hispanic white women, underscores the urgent need to address the root causes."
No surprise the assumption remains that the population is getting fatter because we eat too much and exercise too little - "Because the major contributing causes of insulin resistance, such as obesity, poor dietary intake, and inadequate physical activity, are modifiable, clinical consultation and public health campaigns aimed to improve these health behaviors are needed."
As I've noted previously, it's more than just the calories that are causing our increasing waistlines, alarming rates of diabetes and other diseases, and continued decline in overall health. Until we address what is causing the alarming increase in hyperinsulinemia we're not going to solve the problem.
To be sure, the problem is our diet, but it's not the usual suspects - it's not the calories and it's not the saturated fat. It's what we're avoiding in our diet these days!
The researchers allude to the assumption that it's simply a matter of eating properly, but this completely ignores the fact that a higher increase in the prevalence of hyperinsulinemia was found in men, who the data show, ate less calories in 2000 than they did in 1994 (2618 vs 2666). Not only that, but the 2000 data also showed men ate less fat as both a percentage of calories (33.9% vs 32.1%) and in absolute grams (100g vs 93g); less saturated fat as both a percentage of calories (11.3% vs 10.8%) and in absolute grams (33.5g vs 31.5g); and ate a similar intake of carbohydrate (321.25g vs 320.7g) and slightly less protein (102.6g vs 97.5g).
The fact is, in the NHANES 1999-2000 men ate closer to the dietary recommendations than at any previous period surveyed, yet the prevalence of hyperinsulinemia increased more in men than women (38.3% vs 32.1%) while their diet was supposedly improving. Add to this, even with the slight decrease in calories, the men also got fatter - something explained by a chronic state of hyperinsulinemia and insulin resistance.
In 2002, according to the World Health Organization (WHO) data, 72.2% of adult men (age 15+) in the United States had a BMI greater than 25.
So what's going on?
I've said it before, and I'll say it again - our focus on macronutrients as a percentage of our diet is wrong; our obsession with reducing saturated fat is wrong; and our unwillingness to let the data really tell us what is wrong is going to be our undoing.
Folks, the answer is right in the data itself - if only the researchers would step back and look at it without preconceived assumptions about what we should eat, they'd be able to see the glaring and obvious changes we've made in our diet since at least 1970 that are making us fat and sick.
We're eating too much sugar, too many refined carbohydrates and not nearly enough quality protein.
Ahhh, yes, protein.
I write a lot about protein, don't I?
The reason is that it's not just protein per se that we require, but specific amino acids from foods rich with protein. In fact, the very foods we are told to limit and/or avoid in our diet - eggs, beef, lamb, whole milk and dairy products made from whole milk. We're repeatedly told these foods have too much saturated fat and cholesterol - that we can get our protein from other foods, plant based foods, just as easily.
What we're not told is the additional cost of calories to actually consume enough amino acids, in the amounts we require for those considered "essential," if we're eating plant-based proteins instead of animal based proteins!
For example, two eggs will cost you 142 calories and provide 12.5g of complete protein, that is it has the correct amount of essential amino acids for each gram of protein consumed.
Want the same 12.5g of protein from a plant-based source?
A slice of whole wheat bread costs you 75-calories and provides 3.1g of protein. It's also not a complete source of protein since it has a limited amino acid - an amino acid that isn't high enough to provide enough to complete the ratio needed for "complete" protein. So, you need to add another food with that limited amino acid, like peanut butter. So then, two tablespoons of peanut butter will cost you another 188-calories and provide 8.03g of protein. It too is a limited protein - lacking enough of a different amino acid than the bread, but together they work to provide enough of the amino acids needed. But, also important here - combined they also cost you 263-calories for that 11.3g of protein.
You've now eaten more calories and less protein - 121-calories more, 1g less protein.
Hey, you have eaten less saturated fat and cholesterol - but more carbohydrate, which means you need more insulin to lower your blood sugars as they rise with more carbohydrate.
And, still the researchers are trying to understand why there is an increase in hyperinsulinemia in the adult population? Why we're getting fatter by the year? Why we're seeing more diabetes and complications of high blood sugars and insulin?
Good grief - it's right there is the data!
Our overall diet is WRONG for our metabolism, courtesy of the dietary guidelines of the last thirty years that have persisted in telling us to limit animal foods, eat more plant-based foods and limit cholesterol and saturated fat.
We need to re-appreciate the role of protein in our daily diet - specifically complete protein sources. Until we do we're going to continue to see alarming increases in obesity, insulin resistance, hyperinsulinemia, and diabetes; and watch as our children are afflicted younger and younger.
We are simply not designed to eat the diet recommended; and now, after thirty odd years those recommendations are haunting us - mocking us as we reach for yet another bean burrito or whole grain cereal and skim milk in the mistaken belief it's all about calories in and calories out, making sure we don't eat too much saturated fat and choose more plant-based foods.
Like the canaries in the mine, slowly dying in the presence of odorless but harmful gases, we're slowly dying in the presence of seemingly logical yet harmful dietary recommendations. All the researchers can keep repeating is eat less and move more; while encoraging us to eat more more whole grains, more fruits and vegetables, more skim milk and non-fat dairy, more beans, more soy and limit saturated fat by eating less meat.
Millions of Americans are consciously trying to lose weight and eat a better diet - the data tells us they are indeed trying to and succeeding in reducing fat and calories; it also tells us that in the process of doing this, they're eating less protein and along the way, choosing incomplete sources of protein, thus they're slowly bankrupting their health and well-being for the long-term.
Let's not forget, the more you weigh, the more protein you require each day. So before you jump in with both feet to a diet that restricts your calories and is based on the dietary guidelines - remember this - doing so is going to significantly reduce your protein intake.
Just do the math.
If you weigh 250-pounds, you require (as per the IOM dietary reference intakes) a minimum of 90.9g of complete protein each day. Let's say you're eating 2,500-calories a day with 16% of those calories from protein - then you're eating about 100g of protein each day right now - pretty darn close to what you require each day and most likely just about right when you consider you're eating protein from many different sources, both complete and limited.
Go on a diet based on the recommendation for 1800-calories a day, with 30% fat, 55% carbohydrate and 15% protein, your protein intake just dropped to 67.5g a day - inadequate according to the IOM requirements for protein intake - in fact, you'll be missing your protein requirement by 26% each day.
Now consider this - until you reach a body weight of 185-pounds (lose 65-pounds) that level of protein intake will continue to be chronically inadequate - all the while forcing your metabolism to work with less than it requires each day. We're not talking calories here - we're talking about the protein - the basic building blocks of every cell in your body and enzymes, hormones, immunoglobulins, neurotransmitters, nutrient transport and storage compounds and cell membrane receptors. How long do you really think your body will want to try to function at such a significant metabolic disadvantage?
And researchers are stumped as to why we're growing fatter and sicker?
It's right there, staring us in the face, in the data.
Eat your protein!
Thursday, October 19, 2006
ASRM Conference
I'll be away at the annual ASRM conference in New Orleans, and won't be posting again, most likely, until next Thursday, October 26, 2006! Hope to have you back again soon!
Wednesday, October 18, 2006
One More Reason to Know Where your Food Comes From
Well, if you need more incentive to consider why it's important to know where your food comes from - consider this:
FDA Is Set To Approve Milk, Meat From Clones
Three years after the Food and Drug Administration first hinted that it might permit the sale of milk and meat from cloned animals, prompting public reactions that ranged from curiosity to disgust, the agency is poised to endorse marketing of the mass-produced animals for public consumption.
The decision, expected by the end of this year, is based largely on new data indicating that milk and meat from cloned livestock and their offspring pose no unique risks to consumers."Our evaluation is that the food from cloned animals is as safe as the food we eat every day," said Stephen F. Sundlof, the FDA's chief of veterinary medicine, who has overseen the long-stalled risk assessment.
Farmers and companies that have been growing cloned barnyard animals from single cells in anticipation of a lucrative market say cloning will bring consumers a level of consistency and quality impossible to attain with conventional breeding, making perfectly marbled beef and reliably lean and tasty pork the norm on grocery shelves.
Continue reading article at the Washington Post...
FDA Is Set To Approve Milk, Meat From Clones
Three years after the Food and Drug Administration first hinted that it might permit the sale of milk and meat from cloned animals, prompting public reactions that ranged from curiosity to disgust, the agency is poised to endorse marketing of the mass-produced animals for public consumption.
The decision, expected by the end of this year, is based largely on new data indicating that milk and meat from cloned livestock and their offspring pose no unique risks to consumers."Our evaluation is that the food from cloned animals is as safe as the food we eat every day," said Stephen F. Sundlof, the FDA's chief of veterinary medicine, who has overseen the long-stalled risk assessment.
Farmers and companies that have been growing cloned barnyard animals from single cells in anticipation of a lucrative market say cloning will bring consumers a level of consistency and quality impossible to attain with conventional breeding, making perfectly marbled beef and reliably lean and tasty pork the norm on grocery shelves.
Continue reading article at the Washington Post...
Tuesday, October 17, 2006
Warning - Low-Carb Diets Bad for Diabetics - So Say Researchers!
Where do I even start with this one, published in the October 3 issue of Nutrition? Low-carbohydrate and high-fat intake among adult patients with poorly controlled type 2 diabetes mellitus. (abstract)
It's not really as study per se, but the findings of baseline dietary habits of subjects about to start a trial to investigate dietary intervention to control type II diabetes.
What caught my attention was the conclusion in the abstract, "This dietary pattern may represent a popular trend that extends beyond our particular study and, if so, has serious cardiovascular implications in this vulnerable population of T2DM patients."
What, pray tell, is the dietary pattern in question?
Well, if we rely on publication title and what the researchers tell us, it is a low-carbohydrate diet; not only that, it's this low-carbohydrate dietary pattern reported that is leading the way to cardiovascular complications down the road.
Abstracts like this one should have a warning: Beware, you're about to enter the assumption-spin zone!
You know me....never quite content with the abstract alone, I want to see the data!
How about we take a look?
Wait....
Before I go through the data reported in the study, how about I first review the ADA's definition of what level of carbohydrate intake they consider a low-carbohydrate diet. You'll see in a moment why this definition is important.
From the latest update to the ADA position statement: Nutrition Recommendations and Interventions for Diabetes–2006:
Twice they state the minimum carbohydrate intake levels to consume. First in the energy balance section with "Low-carbohydrate diets (restricting total carbohydrate to less than 130 g/day) are not recommended in the treatment of overweight/obesity;" and again in the nutrition recommendations section with "Low-carbohydrate diets, restricting total carbohydrate to less than 130 g/day, are not recommended in the management of diabetes."
Even before they updated the Standards of Care this summer, their position statement published in January, Standards of Medical Care in Diabetes - 2006, stated "Low-carbohydrate diets (restricting total carbohydrate to less than 130 g/day) are not recommended in the management of diabetes."
So we can see the ADA is firm and clear in the belief that individuals, even those with type II diabetes, must consume at least 130g of carbohydrate each day; otherwise they are consuming a low-carbohydrate diet.
With me so far?
Now in the study above, the researchers specifically cite the same January 2006 position statement as their reference for their statement "Diets that provide low carbohydrate, low fiber, and high saturated fat contribute to disease complications in diabetes and are not recommended [12];" with reference 12 being Standards of Medical Care in Diabetes - 2006. Diabetes Care 2006; 29(suppl 1):S4-42.
I am making a point of this citation because the researchers state their objective in publishing this paper as "...the specific prevalence of low-carbohydrate diet trend in patients with T2DM has not been documented. Thus, the objectives of the present study were to examine baseline dietary, physiologic, and demographic information from adult patients with poorly controlled T2DM in an academic medical center."
So far, so good.
The researchers recruited 163 potential subjects from eight physicians who agreed to participate and help find subjects, along with the use of intranet messages and flyers to find patients willing to participate if the individual's physician cleared them to be screened as a candidate. Then these 163 candidates were included or excluded by telephone interviews, HbA1c screening and inclusion/exclusion criteria. The screening resulted in 40 subjects accepted and enrolled in the Diabetic Education Eating Plan Study.
The exclusion criteria included this curious reason to reject a subject, "Currently adhering to a low-carbohydrate diet such as the Atkins Diet or the South Beach Diet."
The reason given why this would exclude someone from enrollement in the study? From an intervention perspective, this exclusion was because these diets are low in all sources of carbohydrate, and modification of the type of carbohydrate (GI) will have a limited effect on glycemic load (GL) and therefore on HbA1c.
Okay, so those already eating low-carbohydrate diets were excluded because modifying their dietary carbohydrate within the study protocol for GI and GL of carbohydrates won't result in the data showing a benefit to HbA1c.
In fact, this is a very subtle admission that the dietary intervention the researchers are about to subject their participants to is not better for them if they are already following a low-carbohydrate diet.They excluded subjects already doing a low-carbohydrate diet because carbohydrate restricted diets are already low GI and GL; those individuals are already assumed to be benefiting from lower GI and GL, and increasing their carbohydrate actually risks the trial data in the future!
Basically, from what I can see, the researchers excluded these individuals because there is adequate data available that tells them if they modify the diet to be higher in carbohydrate, even though intake will be within the protocol definition of lower GI and GL, these folks will at risk to be negatively affected; and the potential for such would negatively affect the data outcome seeking to show benefit from dietary intervention in the trial.
So then, how did the researchers - after painstakingly excluding those following a low-carbohydrate diet - conclude their study subjects were eating a low-carbohydrate diet?
In their conclusions they state, straight out "All participants stated that they were engaged in dietary management of their diabetes, although they specifically stated they were not currently following on of the popular low-carbohydrate diets and therefore met study criteria"
They reported average intake was 159g carbohydrate per day, it did not fall below the ADA minimum intake of 130g, nor meet the ADA definition of a low-carbohydrate diet, yet these inconvenient facts do not stop the researchers from concluding this was a low-carbohydrate diet.
"Low-carbohydrate and high-fat intakes were observed at baseline among most participants with poorly controlled T2DM at our primary care clinic, despite the exclusion of patients following low-carbohydrate dietary programs such as the Atkins and South Beach diets."
If that wasn't enough, they continued, "Our obervations may be representative of many other patients with T2DM, and perhaps of a trend in the wake of the low-carbohydrate diets. Such a diet likely has cardiovascular implications for patients with T2DM, obesity, hypertension, and hyperlipidemia. Although many researchers are advocating this low-carbohydrate approach to diabetic management, more research is needed to determine the effect of this dietary recommendation on other macronutriets such as saturatred fat and fiber."
Oh, and it keeps getting better - "We found saturated fat intake to be more than twice that of the American Heart Association recommendation. We speculate that, when reducing carbohydrate intake to control weight and hyperglycemia, participants appeared to have replaced the energy they previously got from carbohydrate with energy from fat. Further, participants did not choose to replace carbohydrates with the monnounsaturated or polyunsaturated fats that have been shown to be cardioprotective. The ADA recommends a diet with less than 7% saturated fat content for people with diabetes. It is well understood that saturated fat is one of the main factors contributing to elevation of low-density lipoprotein cholesterol, which can increase risk of cardiovascular disease and overall inflammation."
On the one hand we have a population of subjects that specifically stated they're not following a low-carbohydrate diet and their reported intake of carbohydrate confirms they are eating more than 130g of carbohydrate a day as insisted upon by the ADA; then, on the other we have a team of researchers saying this dietary patten is a low-carbohydrate diet; who then go on to warn of dire consequences, even though their references and citations confirm their subjects are not eating a low-carbohydrate diet.
And this made it through peer-review?
This was accepted and published?
What the baseline data clearly shows is their study population is consuming a crappy diet.
But hey, don't let inconvenient facts deter a good assumption!
The fact is, one simply does not consume an average glycemic index [GI] of 80.7 (based on referent white bread = 100), and glycemic load [GL] of 133.62, if they're following a low-carbohydrate diet. No can do.
Add to that, a carbohydrate intake of an average 159g daily exceeds the ADA minimum of 130g per day!
But, the sad fact is, there is a lot of mileage to be gained if you can find a way to include, talk about and then discredit low-carbohydrate or carbohydrate restricted diets as a therapy for type II diabetes.
Just call whatever it is you find "low-carbohydrate," point out all the negative potential problems you can think of, cite and promote the ADA diet as ideal, and don't forget to ignore all data from the studies available that resulted in statistically significant findings of benefit - and, guess what? You've found the recipe for successful publication these days!
The researchers did not include any acknowledgement of the glaring, fatal flaw in their conclusion that the dietary pattern of their subjects was the cause their elevated HbA1c and concurrent complications. They assumed that it was because of the "low carbohydrate" diet, providing an average 159g of carbohydrate each day.
Why is this a fatal flaw?
The researchers did not investigate their subject populations progression of diabetes since diagnosis. That is, they did not seek to answer the question - are our subjects better or worse today than when they were diagnosed? They didn't seek to know if their subjects diabetes had progressed or improved since diagnosis - instead they assumed the HbA1c at 8.3%, hyperlipidemia, hypertension and other associated complications observed was a consequence of of the reported dietary patten instead of investigating their previous measures of HbA1c, cholesterol, blood pressure, etc.
They simply do not know if their subjects diabetes is worse or better than it was at diagnosis, or at any point previously in their history, because they didn't bother to look.
It was just so much easier to assume the observed complications and poor control were such because the of their dietary pattern.
Intellectual honesty demands we insist researchers accurately reflect their findings in their publications; it means we must not accept shoddy work or warnings of impending doom that are based on nothing more than assumptions.
Because the researchers did not review history or previous test results in their population (HbA1c, cholesterol, blood pressure) to determine if the reported dietary pattern is exacerbating the observed diabetic complications, it is nothing more than an assumption that the reported baseline diet is the reason for their complications.
Quite frankly the data included actually suggests that both quality and absolute gram intake of carbohydrate matters. But saying that would mean suggesting the ADA minimum intake of 130g is too simplistic and perhaps even too high. Remember, they excluded those already consuming a low-carb diet because they would not realize a benefit to their HbA1c in the study underway.
We know - this is something not argued within the diabetes community at all - that carbohydrates directly influence blood sugars; they raise blood sugars. As evidenced by the findings at baseline - when consumption of carbohydrates is such that glycemic index and load is frighteningly high, while absolute gram intake is moderate and above current recommendations, unacceptably high HbA1c (indicative of chronic hyperglycemia), hyperlipidemia, hypertension and other complications may be indicative of an overall poor dietary pattern in patients trying to control blood sugars while meeting ADA minimum intake of 130g or more carbohydrate each day.
But the researchers don't take this approach.
Nor do they acknowledge what they don't know - was this level of carbohydrate and fat, even with higher than desired GI and GL, resulting in improvement or progression of diabetes since diagnosis?
They don't know.
We don't know.
They didn't ask.
They should have.
Or they should have at least acknowledged it was premature to make the assumption the dietary pattern reported for carbohydrates and saturated fat was the cause of the complications observed at baseline in this population.
The bottom line is that this paper is an intellectual disgrace and impedes the progress of science. Perhaps, as a friend of mine suggested this morning an erratum needs to be included to say...the purpose of this study is to examine whether Nutrition is a properly peer-reviwed publication.
It's not really as study per se, but the findings of baseline dietary habits of subjects about to start a trial to investigate dietary intervention to control type II diabetes.
What caught my attention was the conclusion in the abstract, "This dietary pattern may represent a popular trend that extends beyond our particular study and, if so, has serious cardiovascular implications in this vulnerable population of T2DM patients."
What, pray tell, is the dietary pattern in question?
Well, if we rely on publication title and what the researchers tell us, it is a low-carbohydrate diet; not only that, it's this low-carbohydrate dietary pattern reported that is leading the way to cardiovascular complications down the road.
Abstracts like this one should have a warning: Beware, you're about to enter the assumption-spin zone!
You know me....never quite content with the abstract alone, I want to see the data!
How about we take a look?
Wait....
Before I go through the data reported in the study, how about I first review the ADA's definition of what level of carbohydrate intake they consider a low-carbohydrate diet. You'll see in a moment why this definition is important.
From the latest update to the ADA position statement: Nutrition Recommendations and Interventions for Diabetes–2006:
Twice they state the minimum carbohydrate intake levels to consume. First in the energy balance section with "Low-carbohydrate diets (restricting total carbohydrate to less than 130 g/day) are not recommended in the treatment of overweight/obesity;" and again in the nutrition recommendations section with "Low-carbohydrate diets, restricting total carbohydrate to less than 130 g/day, are not recommended in the management of diabetes."
Even before they updated the Standards of Care this summer, their position statement published in January, Standards of Medical Care in Diabetes - 2006, stated "Low-carbohydrate diets (restricting total carbohydrate to less than 130 g/day) are not recommended in the management of diabetes."
So we can see the ADA is firm and clear in the belief that individuals, even those with type II diabetes, must consume at least 130g of carbohydrate each day; otherwise they are consuming a low-carbohydrate diet.
With me so far?
Now in the study above, the researchers specifically cite the same January 2006 position statement as their reference for their statement "Diets that provide low carbohydrate, low fiber, and high saturated fat contribute to disease complications in diabetes and are not recommended [12];" with reference 12 being Standards of Medical Care in Diabetes - 2006. Diabetes Care 2006; 29(suppl 1):S4-42.
I am making a point of this citation because the researchers state their objective in publishing this paper as "...the specific prevalence of low-carbohydrate diet trend in patients with T2DM has not been documented. Thus, the objectives of the present study were to examine baseline dietary, physiologic, and demographic information from adult patients with poorly controlled T2DM in an academic medical center."
So far, so good.
The researchers recruited 163 potential subjects from eight physicians who agreed to participate and help find subjects, along with the use of intranet messages and flyers to find patients willing to participate if the individual's physician cleared them to be screened as a candidate. Then these 163 candidates were included or excluded by telephone interviews, HbA1c screening and inclusion/exclusion criteria. The screening resulted in 40 subjects accepted and enrolled in the Diabetic Education Eating Plan Study.
The exclusion criteria included this curious reason to reject a subject, "Currently adhering to a low-carbohydrate diet such as the Atkins Diet or the South Beach Diet."
The reason given why this would exclude someone from enrollement in the study? From an intervention perspective, this exclusion was because these diets are low in all sources of carbohydrate, and modification of the type of carbohydrate (GI) will have a limited effect on glycemic load (GL) and therefore on HbA1c.
Okay, so those already eating low-carbohydrate diets were excluded because modifying their dietary carbohydrate within the study protocol for GI and GL of carbohydrates won't result in the data showing a benefit to HbA1c.
In fact, this is a very subtle admission that the dietary intervention the researchers are about to subject their participants to is not better for them if they are already following a low-carbohydrate diet.They excluded subjects already doing a low-carbohydrate diet because carbohydrate restricted diets are already low GI and GL; those individuals are already assumed to be benefiting from lower GI and GL, and increasing their carbohydrate actually risks the trial data in the future!
Basically, from what I can see, the researchers excluded these individuals because there is adequate data available that tells them if they modify the diet to be higher in carbohydrate, even though intake will be within the protocol definition of lower GI and GL, these folks will at risk to be negatively affected; and the potential for such would negatively affect the data outcome seeking to show benefit from dietary intervention in the trial.
So then, how did the researchers - after painstakingly excluding those following a low-carbohydrate diet - conclude their study subjects were eating a low-carbohydrate diet?
In their conclusions they state, straight out "All participants stated that they were engaged in dietary management of their diabetes, although they specifically stated they were not currently following on of the popular low-carbohydrate diets and therefore met study criteria"
They reported average intake was 159g carbohydrate per day, it did not fall below the ADA minimum intake of 130g, nor meet the ADA definition of a low-carbohydrate diet, yet these inconvenient facts do not stop the researchers from concluding this was a low-carbohydrate diet.
"Low-carbohydrate and high-fat intakes were observed at baseline among most participants with poorly controlled T2DM at our primary care clinic, despite the exclusion of patients following low-carbohydrate dietary programs such as the Atkins and South Beach diets."
If that wasn't enough, they continued, "Our obervations may be representative of many other patients with T2DM, and perhaps of a trend in the wake of the low-carbohydrate diets. Such a diet likely has cardiovascular implications for patients with T2DM, obesity, hypertension, and hyperlipidemia. Although many researchers are advocating this low-carbohydrate approach to diabetic management, more research is needed to determine the effect of this dietary recommendation on other macronutriets such as saturatred fat and fiber."
Oh, and it keeps getting better - "We found saturated fat intake to be more than twice that of the American Heart Association recommendation. We speculate that, when reducing carbohydrate intake to control weight and hyperglycemia, participants appeared to have replaced the energy they previously got from carbohydrate with energy from fat. Further, participants did not choose to replace carbohydrates with the monnounsaturated or polyunsaturated fats that have been shown to be cardioprotective. The ADA recommends a diet with less than 7% saturated fat content for people with diabetes. It is well understood that saturated fat is one of the main factors contributing to elevation of low-density lipoprotein cholesterol, which can increase risk of cardiovascular disease and overall inflammation."
On the one hand we have a population of subjects that specifically stated they're not following a low-carbohydrate diet and their reported intake of carbohydrate confirms they are eating more than 130g of carbohydrate a day as insisted upon by the ADA; then, on the other we have a team of researchers saying this dietary patten is a low-carbohydrate diet; who then go on to warn of dire consequences, even though their references and citations confirm their subjects are not eating a low-carbohydrate diet.
And this made it through peer-review?
This was accepted and published?
What the baseline data clearly shows is their study population is consuming a crappy diet.
But hey, don't let inconvenient facts deter a good assumption!
The fact is, one simply does not consume an average glycemic index [GI] of 80.7 (based on referent white bread = 100), and glycemic load [GL] of 133.62, if they're following a low-carbohydrate diet. No can do.
Add to that, a carbohydrate intake of an average 159g daily exceeds the ADA minimum of 130g per day!
But, the sad fact is, there is a lot of mileage to be gained if you can find a way to include, talk about and then discredit low-carbohydrate or carbohydrate restricted diets as a therapy for type II diabetes.
Just call whatever it is you find "low-carbohydrate," point out all the negative potential problems you can think of, cite and promote the ADA diet as ideal, and don't forget to ignore all data from the studies available that resulted in statistically significant findings of benefit - and, guess what? You've found the recipe for successful publication these days!
The researchers did not include any acknowledgement of the glaring, fatal flaw in their conclusion that the dietary pattern of their subjects was the cause their elevated HbA1c and concurrent complications. They assumed that it was because of the "low carbohydrate" diet, providing an average 159g of carbohydrate each day.
Why is this a fatal flaw?
The researchers did not investigate their subject populations progression of diabetes since diagnosis. That is, they did not seek to answer the question - are our subjects better or worse today than when they were diagnosed? They didn't seek to know if their subjects diabetes had progressed or improved since diagnosis - instead they assumed the HbA1c at 8.3%, hyperlipidemia, hypertension and other associated complications observed was a consequence of of the reported dietary patten instead of investigating their previous measures of HbA1c, cholesterol, blood pressure, etc.
They simply do not know if their subjects diabetes is worse or better than it was at diagnosis, or at any point previously in their history, because they didn't bother to look.
It was just so much easier to assume the observed complications and poor control were such because the of their dietary pattern.
Intellectual honesty demands we insist researchers accurately reflect their findings in their publications; it means we must not accept shoddy work or warnings of impending doom that are based on nothing more than assumptions.
Because the researchers did not review history or previous test results in their population (HbA1c, cholesterol, blood pressure) to determine if the reported dietary pattern is exacerbating the observed diabetic complications, it is nothing more than an assumption that the reported baseline diet is the reason for their complications.
Quite frankly the data included actually suggests that both quality and absolute gram intake of carbohydrate matters. But saying that would mean suggesting the ADA minimum intake of 130g is too simplistic and perhaps even too high. Remember, they excluded those already consuming a low-carb diet because they would not realize a benefit to their HbA1c in the study underway.
We know - this is something not argued within the diabetes community at all - that carbohydrates directly influence blood sugars; they raise blood sugars. As evidenced by the findings at baseline - when consumption of carbohydrates is such that glycemic index and load is frighteningly high, while absolute gram intake is moderate and above current recommendations, unacceptably high HbA1c (indicative of chronic hyperglycemia), hyperlipidemia, hypertension and other complications may be indicative of an overall poor dietary pattern in patients trying to control blood sugars while meeting ADA minimum intake of 130g or more carbohydrate each day.
But the researchers don't take this approach.
Nor do they acknowledge what they don't know - was this level of carbohydrate and fat, even with higher than desired GI and GL, resulting in improvement or progression of diabetes since diagnosis?
They don't know.
We don't know.
They didn't ask.
They should have.
Or they should have at least acknowledged it was premature to make the assumption the dietary pattern reported for carbohydrates and saturated fat was the cause of the complications observed at baseline in this population.
The bottom line is that this paper is an intellectual disgrace and impedes the progress of science. Perhaps, as a friend of mine suggested this morning an erratum needs to be included to say...the purpose of this study is to examine whether Nutrition is a properly peer-reviwed publication.
Monday, October 16, 2006
Industrial Agriculture Under Fire
Dr. Mike Eades already penned a piece today about the New York Times Magazine article, The Vegetable-Industrial Complex, by Michael Pollan (author of The Omnivore's Dilemma).
No need for repeats - if you haven't already been over there, take a few moments to go read Dr. Eades' Patronize your farmer’s market.
No need for repeats - if you haven't already been over there, take a few moments to go read Dr. Eades' Patronize your farmer’s market.
Researchers: Low-Carb Diet Significantly Reduces Hepatic Fat in NAFLD
Back in March I wrote about a review in the World Journal of Gastroenterology - Non-alcoholic fatty liver disease and the metabolic syndrome: Effects of weightloss and a review of popular diets. Are low carbohydrate diets the answer?; in which researchers noted that carbohydrate restricted diets not only enable weight loss, but are also show "greater improvement in markers of the metabolic syndrome without significant adverse effects with low-carbohydrate diets. This raises the question of whether low-carbohydrate diets should be recommended as part of a weight loss strategy for our patients. At this point, questions regarding the nutritional adequacy and long-term safety remain. While studies have evaluated the effect of these diets on weight loss, cardiovascular and metabolic marker studies are needed to evaluate the effect of these diets specifically on NAFLD [Non-Alcoholic Fatty Liver Disease]."
Last month a study was published in the British Journal of Radiology, Low-carbohydrate diet induced reduction of hepatic lipid content observed with a rapid non-invasive MRI technique, in which researchers investigated non-invasive MRI imaging as a way to measure hepatic fat changes over 10-days in subjects following a low-carbohydrate diet.
While the intent of the study was to determine if MRI imaging is an effective way to measure hepatic fat; the researchers found some statistically significant results in those following a low-carb diet!
All subjects demonstrated significant (p less than 0.01) reductions in hepatic fat by day 10. A strong correlation ( = 0.81) existed between the initial fat content and the percentage fat content reduction in the first 3 days of the diet. All subjects lost weight (average 1.7 kg at day 3 and 3.0 kg at day 10), but this was not correlated with hepatic fat loss after 3 days or 10 days of dieting.
Just more food for the grist mill of thought!
Last month a study was published in the British Journal of Radiology, Low-carbohydrate diet induced reduction of hepatic lipid content observed with a rapid non-invasive MRI technique, in which researchers investigated non-invasive MRI imaging as a way to measure hepatic fat changes over 10-days in subjects following a low-carbohydrate diet.
While the intent of the study was to determine if MRI imaging is an effective way to measure hepatic fat; the researchers found some statistically significant results in those following a low-carb diet!
All subjects demonstrated significant (p less than 0.01) reductions in hepatic fat by day 10. A strong correlation ( = 0.81) existed between the initial fat content and the percentage fat content reduction in the first 3 days of the diet. All subjects lost weight (average 1.7 kg at day 3 and 3.0 kg at day 10), but this was not correlated with hepatic fat loss after 3 days or 10 days of dieting.
Just more food for the grist mill of thought!
Sunday, October 15, 2006
Additional Links
I've once again updated my sidebar links to include three new additions for your reading pleasure!
Over at the Low-Carb Lab, Suzique writes briefs on items of interest and studies related to low-carb diets.
Sherri, at A Pinch Of...blog shares her thoughts and insights on a number of interesting topics for those following a low-carb diet.
And, last but not least, PJ at The Divine LowCarb shares her experiences as she loses weight on a low-carb diet.
As always, if you know of a good blog related to low-carb or controlled-carb, feel free to email me and suggest inclusion in my sidebar. I can't include every blog out there, but when a blog is quality and updated in a timely manner, I will certainly consider it!
Over at the Low-Carb Lab, Suzique writes briefs on items of interest and studies related to low-carb diets.
Sherri, at A Pinch Of...blog shares her thoughts and insights on a number of interesting topics for those following a low-carb diet.
And, last but not least, PJ at The Divine LowCarb shares her experiences as she loses weight on a low-carb diet.
As always, if you know of a good blog related to low-carb or controlled-carb, feel free to email me and suggest inclusion in my sidebar. I can't include every blog out there, but when a blog is quality and updated in a timely manner, I will certainly consider it!
Saturday, October 14, 2006
The Sad Death Of 'Organic'
On the heels of my own missive about the dilution of organic, SFGate.com carried a piece by Mark Morford, The Sad Death Of 'Organic' How weird and depressing is it now that Kellogg's and Wal-Mart are hawking 'natural' foods? yesterday.
I was a little unprepared. The commercial came on and I heard the familiar ukulele strums of the late Hawaiian singer Israel Kamakawiwo'ole's famous and famously beautiful version of "Over the Rainbow" (I know, but it really is quite lovely) and my first reaction was merely to cringe and wince as yet another exquisite and plaintive song was whored out to the advertising demons, just one of thousands.
But then came the barrage of images: the requisite shot of the Perfect Mom feeding her Perfect Child some sort of Perfect Food, all bathed in soft morning breakfasty light with happy trees peeking through the windows of the Perfect Kitchen in some utopian hunk of Perfect America, a bizarre scene that of course does not exist anywhere on this planet given how there weren't three empty wine bottles and some used underwear and a stack of dirty dishes and a fresh bottle of Xanax and an open newspaper offering up giant headlines about murders and nuclear warheads and Korean sex slaves anywhere in sight.
And then it happened. The logo. The product shot. The soothing voice-over. It was a commercial for a brand-new product: Kellogg's Organic Rice Krispies. And your heart goes, Ugh.
Continue reading the article...
I was a little unprepared. The commercial came on and I heard the familiar ukulele strums of the late Hawaiian singer Israel Kamakawiwo'ole's famous and famously beautiful version of "Over the Rainbow" (I know, but it really is quite lovely) and my first reaction was merely to cringe and wince as yet another exquisite and plaintive song was whored out to the advertising demons, just one of thousands.
But then came the barrage of images: the requisite shot of the Perfect Mom feeding her Perfect Child some sort of Perfect Food, all bathed in soft morning breakfasty light with happy trees peeking through the windows of the Perfect Kitchen in some utopian hunk of Perfect America, a bizarre scene that of course does not exist anywhere on this planet given how there weren't three empty wine bottles and some used underwear and a stack of dirty dishes and a fresh bottle of Xanax and an open newspaper offering up giant headlines about murders and nuclear warheads and Korean sex slaves anywhere in sight.
And then it happened. The logo. The product shot. The soothing voice-over. It was a commercial for a brand-new product: Kellogg's Organic Rice Krispies. And your heart goes, Ugh.
Continue reading the article...
Friday, October 13, 2006
STUDY: Lowering LDL Not Supported By Evidence
It should come as no surprise that the recently published conclusion by researchers that there is "no high-quality clinical evidence to support currently proposed treatment goals for LDL cholesterol," is being quietly ignored by most of the popular media outlets.
The review, Narrative Review: Lack of Evidence for Recommended Low-Density Lipoprotein Treatment Targets: A Solvable Problem, was published in the October 3 issue of the Annals of Internal Medicine.
While Forbes did carry an article yesterday about the study - Study Questions Value of Lower Cholesterol Targets, it was simply a reprint of the HealthDay News article; which was a repackaging of the press release from October 2, issued by University of Michigan Health System. In fact, as of today, only 16 articles are available online about this study, and that includes the press release!
And of course, you do have to love this headline from HeartWire - No evidence yet for ultralow LDL-cholesterol levels, according to Michigan researchers. [emphasis mine]
Why ignore this study?
Could it be that "[a]fter performing an exhaustive review of existing research on LDL cholesterol and heart health, they [the researchers] conclude that there is no scientifically valid evidence to support the ultra-low LDL target of 70 milligrams/deciliter for very high-risk patients that has been advocated by some members of the federal government’s National Cholesterol Education Program. Further, they suggest that the evidence previously cited to support an LDL goal of less than 100mg/dL for high risk patients also has major flaws;" every marketing and advertising campaign for statins would need a major over-haul?
Just a quick review of the Lipitor webpage detailing how Lipitor lowers LDL cholesterol gives us a clue why Pfizer and others are not jumping up and down with this finding.
If they remain quiet, the public may not hear about how the researchers found "For those with LDL cholesterol levels less than 3.36 mmol/L (less than 130 mg/dL), the authors found no clinical trial subgroup analyses or valid cohort or case–control analyses suggesting that the degree to which LDL cholesterol responds to a statin independently predicts the degree of cardiovascular risk reduction."
This review shatters the diet-heart hypothesis by exposing the theory as unsupported by the evidence.
Now, you may wonder if these researchers are "those quacks" who simply refuse to accept the conventional wisdom that has repeated for decades lowering LDL is important to reduce risks.
Think again.
Back in April 2004, two of the three scientists who conducted this review specifically recommended and supported the use of statins to lower LDL cholesterol to reduce risk. In their previous work, also published in the Annals of Internal Medicine, Pharmacologic Lipid-Lowering Therapy in Type 2 Diabetes Mellitus: Background Paper for the American College of Physicians, they concluded, "Most patients, including those whose baseline low-density lipoprotein cholesterol levels are below 2.97 mmol/L (less than115/mg/dL) and possibly below 2.59 mmol/L (less than 100 mg/dL), benefit from statins. Moderate doses of these drugs suffice in most patients with diabetes."
So these were not nay-sayers about statin therapy. Nor are they now. In fact, in the newly published paper, they specifically go to great lengths to continue recommending statins - not to lower LDL, but because of the "known lipid-independent effects of statins."
In their review of the evidence to find support for the use of statins as a therapy to reduce LDL, and thus reduce the presumed risk from elevated LDL, they found major flaws in the data published, including:
The review, Narrative Review: Lack of Evidence for Recommended Low-Density Lipoprotein Treatment Targets: A Solvable Problem, was published in the October 3 issue of the Annals of Internal Medicine.
While Forbes did carry an article yesterday about the study - Study Questions Value of Lower Cholesterol Targets, it was simply a reprint of the HealthDay News article; which was a repackaging of the press release from October 2, issued by University of Michigan Health System. In fact, as of today, only 16 articles are available online about this study, and that includes the press release!
And of course, you do have to love this headline from HeartWire - No evidence yet for ultralow LDL-cholesterol levels, according to Michigan researchers. [emphasis mine]
Why ignore this study?
Could it be that "[a]fter performing an exhaustive review of existing research on LDL cholesterol and heart health, they [the researchers] conclude that there is no scientifically valid evidence to support the ultra-low LDL target of 70 milligrams/deciliter for very high-risk patients that has been advocated by some members of the federal government’s National Cholesterol Education Program. Further, they suggest that the evidence previously cited to support an LDL goal of less than 100mg/dL for high risk patients also has major flaws;" every marketing and advertising campaign for statins would need a major over-haul?
Just a quick review of the Lipitor webpage detailing how Lipitor lowers LDL cholesterol gives us a clue why Pfizer and others are not jumping up and down with this finding.
If they remain quiet, the public may not hear about how the researchers found "For those with LDL cholesterol levels less than 3.36 mmol/L (less than 130 mg/dL), the authors found no clinical trial subgroup analyses or valid cohort or case–control analyses suggesting that the degree to which LDL cholesterol responds to a statin independently predicts the degree of cardiovascular risk reduction."
This review shatters the diet-heart hypothesis by exposing the theory as unsupported by the evidence.
Now, you may wonder if these researchers are "those quacks" who simply refuse to accept the conventional wisdom that has repeated for decades lowering LDL is important to reduce risks.
Think again.
Back in April 2004, two of the three scientists who conducted this review specifically recommended and supported the use of statins to lower LDL cholesterol to reduce risk. In their previous work, also published in the Annals of Internal Medicine, Pharmacologic Lipid-Lowering Therapy in Type 2 Diabetes Mellitus: Background Paper for the American College of Physicians, they concluded, "Most patients, including those whose baseline low-density lipoprotein cholesterol levels are below 2.97 mmol/L (less than115/mg/dL) and possibly below 2.59 mmol/L (less than 100 mg/dL), benefit from statins. Moderate doses of these drugs suffice in most patients with diabetes."
So these were not nay-sayers about statin therapy. Nor are they now. In fact, in the newly published paper, they specifically go to great lengths to continue recommending statins - not to lower LDL, but because of the "known lipid-independent effects of statins."
In their review of the evidence to find support for the use of statins as a therapy to reduce LDL, and thus reduce the presumed risk from elevated LDL, they found major flaws in the data published, including:
- Not Considering Alternative Hypotheses When Interpreting Experiments
- Mistaking Cohort Analyses for True Experimental Results
- Cohort Analyses Using Clinical Trial Data Must Control for Exposure to the Treatment
- The "Healthy Volunteer" Effect Can Severely Bias Studies Evaluating Treatment Targets
- Ecological Comparisons Are a Very Weak Source of Evidence and
- Framing Treatment Goals as False Dichotomies
This review is one that I consider a "must read" for a number of reasons, including it lays out, piece by piece, how a review should be conducted and what to look for nicely; it was well done and included both experimental and clinical trials; and it exposes the problem assumptions, bias and interpretation can cause, especially over years when no challenge to the hypothesis is accepted.
Real science demands we challenge our beliefs and assumptions - for decades now we've watched as targets were repeatedly lowered the target for cholesterol without any clear, convincing data - while we've been repeatedly told there is data to support each and every decision to lower the targets! All the while, there have been scientists, researchers and medical professionals asking "where's the data?" as they're disparaged, dismissed and mocked for challenging the powers that be.
As is clear in this review, lowering LDL cholesterol below 130 or below 100 or below the new target of 70, has no support in the data, is not based on evidence and is a target without foundation for the marketing or promotion of statins.
But, you're not going to hear about it in the news tonight, nor will your doctor.
Heck, you may want to print a copy of the paper to give to your doctor next time he suggests you start taking a stating to lower your LDL cholesterol to reduce your risks!
Thursday, October 12, 2006
Why Organic?
You've probably noticed by now that I often recommend you choose organic foods when your budget allows - most strongly for dairy products, eggs, meats and poultry. The reason is these foods have different fat and nutritional profiles when compared with conventional, industrial farmed foods; with the caveat that the difference is when the animals are provided their natural diet. With regard to plant-based foods - fruits, vegetables, grains, legumes, nuts and seeds, I make the recommendation to choose organic when you can because conventionally grown is usually higher with residue from chemical fertilizers and pesticides.
As the popularity of organic food continues to grow, it seems we're losing something along the way.
Business Week reported this week in The Organic Myth, "[a]s food companies scramble to find enough organically grown ingredients, they are inevitably forsaking the pastoral ethos that has defined the organic lifestyle.
For some companies, it means keeping thousands of organic cows on industrial-scale feedlots. For others, the scarcity of organic ingredients means looking as far afield as China, Sierra Leone, and Brazil -- places where standards may be hard to enforce, workers' wages and living conditions are a worry, and, say critics, increased farmland sometimes comes at a cost to the environment."
Front and center in the article was Stonyfield Farms sourcing powdered milk from New Zealand to make organic yogurt. "Stonyfield's organic farm is long gone. Its main facility is a state-of-the-art industrial plant just off the airport strip in Londonderry, N.H., where it handles milk from other farms. And consider this: Sometime soon a portion of the milk used to make that organic yogurt may be taken from a chemical-free cow in New Zealand, powdered, and then shipped to the U.S."
The CEO and Chairman of Stonyfield, Gary Hirshberg, said "It would be great to get all of our food within a 10-mile radius of our house, [b]ut once you're in organic, you have to source globally."
I don't know about you, but one reason, years ago, I decided to buy organic was to support the foundational principle of organic farming - sustainable agricultural practices.
Like many who learn about how we grow crops and raise animals for food, I was disturbed by some of the conventional farming practices - namely the confinement of animals, fed a diet they'd never consume willingly; the heavy use of industrial fertilizers that deplete soil; and the reality that we were dependent upon so few major crops in the United States. The alarming reality is the majority of our farm land is used to grow field corn, soybeans and wheat; each within an intensive monoculture that limits crop rotation and relies on a the use of more genetically modified seeds along with more pesticides and fertilizers to keep the crop yeilds high.
I never, in my wildest dreams, ever thought I'd be someone who might be labeled a tree-hugger or crunchy granola, but here I am today worried about what we're doing to the environment and our future food supply.
The unfortunate reality is, that as organic continues to grow in popularity, it too is being industrialized with its definition diluted in order to meet the demand of marketing to the masses. As Business Week points out, "...the organic paradox: The movement's adherents have succeeded beyond their wildest dreams, but success has imperiled their ideals."
While Stoneyfield's Hirshberg chalks this up to as "[o]rganic is growing up," the reality is organic is losing its soul as it adopts the very "industrial-agriculture" and "factory farming" practices it once held as out-of-whack with nature, harmful to the environment and unsustainable, to capture marketshare and enhance profitability.
Which leaves me with the question - what should I do?
If organic is to be encouraged to become the dominant farming practice in the US, need I accept compromise is necessary and continue to support its growth by continuing to purchase foods from companies that are gaining a share in the marketplace and therefore be in a better position to exert pressure to change farming practices for the better?
Afterall, it can be argued that land farmed with less pesticide and chemical fertilizer is better than what we're doing now; and that animals raised on organic feed are exposed to less chemical residue from those pesticides and chemical fertrilizers and aren't routinely given hormones and antibiotics.
That does sound like it's better, doesn't it?
Then again, I find myself asking, are the organic practices leading to growth exerting pressure on conventional farming to change, or has conventional farming exerted pressure on organic to change; which is what is driving growth in the sector?
When that question is asked, it's pretty clear to me that organic is changing to adopt more conventional and industrial practices to grow in the marketplace and enhance profits.
Which leaves me with the decision of where to spend my money now and in the future.
After giving thought the pros and cons of continuing to support companies making compromises that move them toward higher profits because of their compromise to an unsustainable model, I've decided to opt-out of the Wall Streetization of organic and let my dollars speak - my money is going to local farmers committed to sustainable agricultural practices.
My reason is simply that for years we've made significant sacrifices in our budget to buy organic - a decision made years ago to support sustainable agriculture.
As anyone who has shopped at Whole Foods, Wild Oats, or natural food/health specialty market can tell you, it's not an inexpensive way to eat.
Years ago the majority of foods available in these stores was primarily sourced from local farmers, ranchers and artisans. Over the years the changes have been subtle, almost imperceptible, as the popularity of organic has grown and demand has increased - more products are on the shelves, a large number of retail chain supermarkets now include a separate organic section to shop in, and the selection year-round is impressive.
Unlike the avilability years ago, today organic fruits and vegetables once difficult to find off-season are readily available year-round; any cut of certified organic meat or poultry, or wild caught seafood you desire is on-hand day-in-day-out; and the variety of organic packaged processed foods often shunned as "unhealthy" - think potato chips, candy bars, soda, etc - line the shelves for our convenience.Indeed, organic has grown up!
It's now a model of industrial agriculture, a shining example of our human cleverness, certified organic, of course.
As a society, we need the guts to do the right thing.
I'm stepping up today and doing what I believe is the right thing - I'm saying no to industrial organic and going to support local farmers committed to sustainable agriculture - the primary reason I went organic years ago.
If you too want to see your money spent to effectively encourage sustainable agriculture, start by simply finding local farmers and ranchers in your area. Two excellent resources online:
EatWild.com
LocalHarvest.org
Keep in mind, that's just your first step. Next you should take the time to get to know these people - visit their farms, ask questions, learn about why they are farmers, and learn why they're committed to sustainable agriculture. If you do that, you'll definitely find room in your budget to support these hard working folks!
I'm going to close with the words of Joel Salatin, an incredible farmer who provided my eggs and chickens when I lived in northern Virginia, "Balancing our ecology, economics, and emotions provides enough challenge to last a lifetime. We never reach a magical destination in this quest for balance, a point in time where we can say 'I've arrived.'"
I know my decision to opt-out of supporting this "grown-up" industrialized organic won't make much difference; there simply is no easy answer, nor perfect solution. I'm just one person making the buying decisions for one family; that, I must admit, will still have to include some compromise along the way.
But, as one person, I can also reach those of you reading here and hope you'll take the time to read more, learn more and decide how you too will spend your dollars as you make buying decisions to feed yourself and your family.
What made organic "grow up" was "one + one + one," a growing number of individuals learning about the unsustainable agricultural practices of conventional farming who grew in a number large to support change through their spending habits. Unfortunately that change isn't exactly in the direction anticipated and expected.
What can and will still speak volumes is the power of the almighty dollar.
One + one + one + one...
Where do you want to invest your hard earned money?
For me, the future is Beyond Organic.
As the popularity of organic food continues to grow, it seems we're losing something along the way.
Business Week reported this week in The Organic Myth, "[a]s food companies scramble to find enough organically grown ingredients, they are inevitably forsaking the pastoral ethos that has defined the organic lifestyle.
For some companies, it means keeping thousands of organic cows on industrial-scale feedlots. For others, the scarcity of organic ingredients means looking as far afield as China, Sierra Leone, and Brazil -- places where standards may be hard to enforce, workers' wages and living conditions are a worry, and, say critics, increased farmland sometimes comes at a cost to the environment."
Front and center in the article was Stonyfield Farms sourcing powdered milk from New Zealand to make organic yogurt. "Stonyfield's organic farm is long gone. Its main facility is a state-of-the-art industrial plant just off the airport strip in Londonderry, N.H., where it handles milk from other farms. And consider this: Sometime soon a portion of the milk used to make that organic yogurt may be taken from a chemical-free cow in New Zealand, powdered, and then shipped to the U.S."
The CEO and Chairman of Stonyfield, Gary Hirshberg, said "It would be great to get all of our food within a 10-mile radius of our house, [b]ut once you're in organic, you have to source globally."
I don't know about you, but one reason, years ago, I decided to buy organic was to support the foundational principle of organic farming - sustainable agricultural practices.
Like many who learn about how we grow crops and raise animals for food, I was disturbed by some of the conventional farming practices - namely the confinement of animals, fed a diet they'd never consume willingly; the heavy use of industrial fertilizers that deplete soil; and the reality that we were dependent upon so few major crops in the United States. The alarming reality is the majority of our farm land is used to grow field corn, soybeans and wheat; each within an intensive monoculture that limits crop rotation and relies on a the use of more genetically modified seeds along with more pesticides and fertilizers to keep the crop yeilds high.
I never, in my wildest dreams, ever thought I'd be someone who might be labeled a tree-hugger or crunchy granola, but here I am today worried about what we're doing to the environment and our future food supply.
The unfortunate reality is, that as organic continues to grow in popularity, it too is being industrialized with its definition diluted in order to meet the demand of marketing to the masses. As Business Week points out, "...the organic paradox: The movement's adherents have succeeded beyond their wildest dreams, but success has imperiled their ideals."
While Stoneyfield's Hirshberg chalks this up to as "[o]rganic is growing up," the reality is organic is losing its soul as it adopts the very "industrial-agriculture" and "factory farming" practices it once held as out-of-whack with nature, harmful to the environment and unsustainable, to capture marketshare and enhance profitability.
Which leaves me with the question - what should I do?
If organic is to be encouraged to become the dominant farming practice in the US, need I accept compromise is necessary and continue to support its growth by continuing to purchase foods from companies that are gaining a share in the marketplace and therefore be in a better position to exert pressure to change farming practices for the better?
Afterall, it can be argued that land farmed with less pesticide and chemical fertilizer is better than what we're doing now; and that animals raised on organic feed are exposed to less chemical residue from those pesticides and chemical fertrilizers and aren't routinely given hormones and antibiotics.
That does sound like it's better, doesn't it?
Then again, I find myself asking, are the organic practices leading to growth exerting pressure on conventional farming to change, or has conventional farming exerted pressure on organic to change; which is what is driving growth in the sector?
When that question is asked, it's pretty clear to me that organic is changing to adopt more conventional and industrial practices to grow in the marketplace and enhance profits.
Which leaves me with the decision of where to spend my money now and in the future.
After giving thought the pros and cons of continuing to support companies making compromises that move them toward higher profits because of their compromise to an unsustainable model, I've decided to opt-out of the Wall Streetization of organic and let my dollars speak - my money is going to local farmers committed to sustainable agricultural practices.
My reason is simply that for years we've made significant sacrifices in our budget to buy organic - a decision made years ago to support sustainable agriculture.
As anyone who has shopped at Whole Foods, Wild Oats, or natural food/health specialty market can tell you, it's not an inexpensive way to eat.
Years ago the majority of foods available in these stores was primarily sourced from local farmers, ranchers and artisans. Over the years the changes have been subtle, almost imperceptible, as the popularity of organic has grown and demand has increased - more products are on the shelves, a large number of retail chain supermarkets now include a separate organic section to shop in, and the selection year-round is impressive.
Unlike the avilability years ago, today organic fruits and vegetables once difficult to find off-season are readily available year-round; any cut of certified organic meat or poultry, or wild caught seafood you desire is on-hand day-in-day-out; and the variety of organic packaged processed foods often shunned as "unhealthy" - think potato chips, candy bars, soda, etc - line the shelves for our convenience.Indeed, organic has grown up!
It's now a model of industrial agriculture, a shining example of our human cleverness, certified organic, of course.
As a society, we need the guts to do the right thing.
I'm stepping up today and doing what I believe is the right thing - I'm saying no to industrial organic and going to support local farmers committed to sustainable agriculture - the primary reason I went organic years ago.
If you too want to see your money spent to effectively encourage sustainable agriculture, start by simply finding local farmers and ranchers in your area. Two excellent resources online:
EatWild.com
LocalHarvest.org
Keep in mind, that's just your first step. Next you should take the time to get to know these people - visit their farms, ask questions, learn about why they are farmers, and learn why they're committed to sustainable agriculture. If you do that, you'll definitely find room in your budget to support these hard working folks!
I'm going to close with the words of Joel Salatin, an incredible farmer who provided my eggs and chickens when I lived in northern Virginia, "Balancing our ecology, economics, and emotions provides enough challenge to last a lifetime. We never reach a magical destination in this quest for balance, a point in time where we can say 'I've arrived.'"
I know my decision to opt-out of supporting this "grown-up" industrialized organic won't make much difference; there simply is no easy answer, nor perfect solution. I'm just one person making the buying decisions for one family; that, I must admit, will still have to include some compromise along the way.
But, as one person, I can also reach those of you reading here and hope you'll take the time to read more, learn more and decide how you too will spend your dollars as you make buying decisions to feed yourself and your family.
What made organic "grow up" was "one + one + one," a growing number of individuals learning about the unsustainable agricultural practices of conventional farming who grew in a number large to support change through their spending habits. Unfortunately that change isn't exactly in the direction anticipated and expected.
What can and will still speak volumes is the power of the almighty dollar.
One + one + one + one...
Where do you want to invest your hard earned money?
For me, the future is Beyond Organic.
Losing Our Minds from Obesity?
We live in a time when two of every three adults is overweight or obese; its also a growing problem across the the globe. Because of its prevalence, it should come as no surprise that obesity is correlated with so many health problems. For years we've seen data telling us that obesity puts us at greater risk for diabetes, heart disease, cancer, and a host of other ailments.
A study, reported by UPI and published in the October 10 issue of Neurology, found "excess weight could impair memory."
Which prompted one of the researchs, Dr. Maxime Cournot, to suggest "Our results can have an additional motivational effect to modify health habits in people who are overweight."
While I agree that overweight and obesity can indeed influence our health, I'm not convinced it is the excess weight alone that increases risk for health issues. In fact, I'm convinced we must dig deeper and address what causes obesity and the development of disease.
My perspective is built upon the understood 'correlation is not causation;' if we're living in a time when more people are overweight and obese, it's a given we'll statistically find more health issues in those who are overweight or obese - there are more people in that category!
Of course the simple answer to our problematic obesity is too many calories in and not enough energy expended each day. Simple answers have simple solutions - eat less move more - is the one we hear most often. Yet that solution has done little to slow the continued rise in obesity in the US, and now we're experiencing a global rise in obesity too.
You may recall my post from September 26 - Of Death and Diabetes - about a study published that was criticized when researchers suggested their findings showed obesity alone was not a risk factor for premature death, but obesity related to diabetes was. The finding is contrary to our intuitive belief that being overweight is unhealthy.
Let me be very clear - being overweight or obese most certainly can be unhealthy and raise the risk of disease and death; but data is showing that the risk is increased in the presence of metabolic disturbance. The risk in the presence of a metabolic disturbance is similar even in those who are not overweight or obese as the data shows in The role of body mass index and diabetes in the development of acute organ failure and subsequent mortality in an observational cohort.
So while the media is hot on the trail of reporting all the negative effects of being overweight, in an effort to motivate or scare us to lose weight, these reports aren't telling us much since it's pretty much expected we'll find more risk being obese or overweight because there are more obese and overweight people in the population.
In the UPI article, it was noted that "excess weight can also lead to poorer management of the body's insulin, which in turn could affect brain cells."
How about this instead - a diet which increases the incidence of episodes of hyperinsulinemia, increases propensity to store excess energy as fat, which increases body weight and risk of overweight and obesity. As this situation is exacerbated and the hyperinsulinemia remains uncontrolled, brain cells are affected by the high levels of insulin, thus affecting cognitive function. Solution - reduce intake of foods that stimulate high levels of insulin to allow the body to burn stored fat as energy, allow a reduction in body weight and restore hormone levels back to normal and reduce the risk of health problems caused by metabolic distrubances.
Oh wait, that would mean we'd have to seriously consider a carbohydrate restricted dietary approach, one that virtually eliminates refined carbohydrates in favor of whole foods, encourages adequate intake of protein and natural fats, if we really wanted to address the underlying issue of overweight, obesity and the concurrent metabolic disturbances.
Truth be told, we'd have to abandon our current dietary habits and long-held beliefs and adopt a diet that is in synch with our metabolism and essential nutrient requirements.
Sadly such advice isn't going to be making the headlines any time soon - instead we'll continue to see the population blamed for their obesity and their health problems; and we'll continue to hear the same-old same-old advice - lose weight, eat less and move more, even though this advice hasn't made a dent in our obesity epidemic, and won't anytime soon.
A study, reported by UPI and published in the October 10 issue of Neurology, found "excess weight could impair memory."
Which prompted one of the researchs, Dr. Maxime Cournot, to suggest "Our results can have an additional motivational effect to modify health habits in people who are overweight."
While I agree that overweight and obesity can indeed influence our health, I'm not convinced it is the excess weight alone that increases risk for health issues. In fact, I'm convinced we must dig deeper and address what causes obesity and the development of disease.
My perspective is built upon the understood 'correlation is not causation;' if we're living in a time when more people are overweight and obese, it's a given we'll statistically find more health issues in those who are overweight or obese - there are more people in that category!
Of course the simple answer to our problematic obesity is too many calories in and not enough energy expended each day. Simple answers have simple solutions - eat less move more - is the one we hear most often. Yet that solution has done little to slow the continued rise in obesity in the US, and now we're experiencing a global rise in obesity too.
You may recall my post from September 26 - Of Death and Diabetes - about a study published that was criticized when researchers suggested their findings showed obesity alone was not a risk factor for premature death, but obesity related to diabetes was. The finding is contrary to our intuitive belief that being overweight is unhealthy.
Let me be very clear - being overweight or obese most certainly can be unhealthy and raise the risk of disease and death; but data is showing that the risk is increased in the presence of metabolic disturbance. The risk in the presence of a metabolic disturbance is similar even in those who are not overweight or obese as the data shows in The role of body mass index and diabetes in the development of acute organ failure and subsequent mortality in an observational cohort.
So while the media is hot on the trail of reporting all the negative effects of being overweight, in an effort to motivate or scare us to lose weight, these reports aren't telling us much since it's pretty much expected we'll find more risk being obese or overweight because there are more obese and overweight people in the population.
In the UPI article, it was noted that "excess weight can also lead to poorer management of the body's insulin, which in turn could affect brain cells."
How about this instead - a diet which increases the incidence of episodes of hyperinsulinemia, increases propensity to store excess energy as fat, which increases body weight and risk of overweight and obesity. As this situation is exacerbated and the hyperinsulinemia remains uncontrolled, brain cells are affected by the high levels of insulin, thus affecting cognitive function. Solution - reduce intake of foods that stimulate high levels of insulin to allow the body to burn stored fat as energy, allow a reduction in body weight and restore hormone levels back to normal and reduce the risk of health problems caused by metabolic distrubances.
Oh wait, that would mean we'd have to seriously consider a carbohydrate restricted dietary approach, one that virtually eliminates refined carbohydrates in favor of whole foods, encourages adequate intake of protein and natural fats, if we really wanted to address the underlying issue of overweight, obesity and the concurrent metabolic disturbances.
Truth be told, we'd have to abandon our current dietary habits and long-held beliefs and adopt a diet that is in synch with our metabolism and essential nutrient requirements.
Sadly such advice isn't going to be making the headlines any time soon - instead we'll continue to see the population blamed for their obesity and their health problems; and we'll continue to hear the same-old same-old advice - lose weight, eat less and move more, even though this advice hasn't made a dent in our obesity epidemic, and won't anytime soon.
Tuesday, October 03, 2006
Omega-3 and Omega-6 Food Sources
Finding information about how much omega-3 and omega-6 fatty acids are in a food or oil isn't an easy undertaking. The information is not all that readily available and takes some time to find. Below is the start of a list of foods and fats/oils to start with - as I find more information, I'll update here and include the sources of the additional information. For now, I wanted to provide a list to start with from the information I have gathered. I ask my readers to add to this list in the comments section - place links and any levels of omega-3/6 tested in the comments for other readers to use!
FATS AND OILS (per 100g)
Fish Oils (average cod, halibut, mackerel, rockfish and salmon oils)
1.2g LA (n-6)
0.9g ALA (n-3)
9.9g EPA (n-3)
12.8g DHA (n-3)
Fish Liver Oil (Atlantic Cod)
1.5g LA (n-6)
0.9g ALA (n-3)
8g EPA (n-3)
14.3 DHA (n-3)
Shellfish Oil (Pacific Oyster)
1.2g LA (n-6)
1.6g ALA (n-3)
21.5g EPA (n-3)
20.2g DHA (n-3)
Nut and Seed Oils
Cashew Oil
16g LA (n-6)
0.4g ALA (n-3)
Peanut Oil
29g LA (n-6)
1.1g ALA (n-3)
Pumpkin SeedOil
51g LA (n-6)
0 ALA (n-3)
Sesame Seed Oil
42g LA (n-6)
0.5g ALA (n-3)
Sunflower Oil
53g LA (n-6)
0g ALA (n-3)
Coconut Oil
3g LA (n-6)
0g ALA (n-3)
Flaxseed Oil
15g LA (n-6)
55g ALA (n-3)
Olive Oil
9g LA (n-6)
0.7g ALA (n-3)
Avocado Oil
12.5g LA (n-6)
1g ALA (n-3)
Macadamia Nut Oil
1.5g LA (n-6)
1.5g ALA (n-3)
Vegetable Oils
Corn Oil
57g LA (n-6)
0.8g ALA (n-3)
Cottonseed Oil
48g LA (n-6)
0.4g ALA (n-3)
Canola Oil
22g LA (n-6)
11g ALA (n-3)
Soybean Oil
53g LA (n-6)
7g ALA (n-3)
Walnut Oil
62g LA (n-6)
4g ALA (n-3)
Wheat Germ Oil
54g LA (n-6)
7g ALA (n-3)
Animal Fats
Beef Tallow (grain-fed beef source)
4g LA (n-6)
0.7g ALA (n-3)
Chicken Fat
17g LA (n-6)
1.1g ALA (n-3)
Lard
10g LA (n-6)
1.4g ALA (n-3)
Mutton Fat
5g LA (n-6)
2.9g ALA (n-3)
WHOLE FOOD SOURCES (per 100g)
Dairy
Cheddar cheese, natural
0.5g LA (n-6)
0.4g ALA (n-3)
Cream cheese, regular
0.8g LA (n-6)
0.5g ALA (n-3)
Gruyere cheese, regular
1.3g LA (n-6)
0.4g ALA (n-3)
American cheese, regular
0.6g LA (n-6)
0.3g ALA (n-3)
Heavy Cream, conventional, grain-fed cows
0.9g LA (n-6)
0.6g ALA (n-3)
Light Cream, conventional, grain-fed cows
0.5g LA (n-6)
0.3g ALA (n-3)
Sour Cream, conventional
0.4g LA (n-6)
0.3g ALA (n-3)
Milk, whole, conventional
0.1g LA (n-6)
0.1g ALA (n-3)
Yogurt, plain, whole milk, conventional
0.1g LA (n-6)
0.1g ALA (n-3)
Egg Yolks, conventional (100g = approximately 4 yolks)
2.6g LA (n-6)
0.05g ALA (n-3)
Egg Yolks, pastured or flaxseed included in diet
4.2g LA (n-6)
2.1g ALA (n-3)
Butter, conventional
2.73g LA (n-6)
0.32g ALA (n-3)
Butter, grass-fed organic
1.8g LA (n-6)
1.2g ALA (n-3)
Meats & Game
Elk
0.343g (n-6)
0.056g (n-3)
Bison
0.156g (n-6)
0.026g (n-3)
Beef, grass-fed
0.139g (n-6)
0.052g (n-3)
Beef, grain-fed, conventional
0.275g (n-6)
0.016g (n-3)
UPDATE - October 5, 2006
Venison, roast, cooked, braised (approximate levels)
0.13g (n-6)
0.06g (n-3)
Sources:
Medeiro, L.C. 2002. Nutritional content of game meat. B-920R. College of Agriculture, University of WyomingUSDA Nutrient Database
Asia Pac J Clin Nutr. 2006;15(1):21-9; Effect of feeding systems on omega-3 fatty acids, conjugated linoleic acid and trans fatty acids in Australian beef cuts: potential impact on human health
Lipids. 2005 Feb;40(2):191-202; A study on the causes for the elevated n-3 fatty acids in cows' milk of alpine origin
Asia Pac J Clin Nutr. 2003;12 Suppl:S38; Feeding regimes affect fatty acid composition in Australian beef cattle
J Nutr Health Aging. 2005 Jul-Aug;9(4):232-42; Where to find omega-3 fatty acids and how feeding animals with diet enriched in omega-3 fatty acids to increase nutritional value of derived products for human: what is actually useful?
Poult Sci. 2000 Jul;79(7):971-4; Enriched eggs as a source of N-3 polyunsaturated fatty acids for humans
Omega-3 Oils - A Practical Guide, Donald Rudin, MD, Clara Felix
FATS AND OILS (per 100g)
Fish Oils (average cod, halibut, mackerel, rockfish and salmon oils)
1.2g LA (n-6)
0.9g ALA (n-3)
9.9g EPA (n-3)
12.8g DHA (n-3)
Fish Liver Oil (Atlantic Cod)
1.5g LA (n-6)
0.9g ALA (n-3)
8g EPA (n-3)
14.3 DHA (n-3)
Shellfish Oil (Pacific Oyster)
1.2g LA (n-6)
1.6g ALA (n-3)
21.5g EPA (n-3)
20.2g DHA (n-3)
Nut and Seed Oils
Cashew Oil
16g LA (n-6)
0.4g ALA (n-3)
Peanut Oil
29g LA (n-6)
1.1g ALA (n-3)
Pumpkin SeedOil
51g LA (n-6)
0 ALA (n-3)
Sesame Seed Oil
42g LA (n-6)
0.5g ALA (n-3)
Sunflower Oil
53g LA (n-6)
0g ALA (n-3)
Coconut Oil
3g LA (n-6)
0g ALA (n-3)
Flaxseed Oil
15g LA (n-6)
55g ALA (n-3)
Olive Oil
9g LA (n-6)
0.7g ALA (n-3)
Avocado Oil
12.5g LA (n-6)
1g ALA (n-3)
Macadamia Nut Oil
1.5g LA (n-6)
1.5g ALA (n-3)
Vegetable Oils
Corn Oil
57g LA (n-6)
0.8g ALA (n-3)
Cottonseed Oil
48g LA (n-6)
0.4g ALA (n-3)
Canola Oil
22g LA (n-6)
11g ALA (n-3)
Soybean Oil
53g LA (n-6)
7g ALA (n-3)
Walnut Oil
62g LA (n-6)
4g ALA (n-3)
Wheat Germ Oil
54g LA (n-6)
7g ALA (n-3)
Animal Fats
Beef Tallow (grain-fed beef source)
4g LA (n-6)
0.7g ALA (n-3)
Chicken Fat
17g LA (n-6)
1.1g ALA (n-3)
Lard
10g LA (n-6)
1.4g ALA (n-3)
Mutton Fat
5g LA (n-6)
2.9g ALA (n-3)
WHOLE FOOD SOURCES (per 100g)
Dairy
Cheddar cheese, natural
0.5g LA (n-6)
0.4g ALA (n-3)
Cream cheese, regular
0.8g LA (n-6)
0.5g ALA (n-3)
Gruyere cheese, regular
1.3g LA (n-6)
0.4g ALA (n-3)
American cheese, regular
0.6g LA (n-6)
0.3g ALA (n-3)
Heavy Cream, conventional, grain-fed cows
0.9g LA (n-6)
0.6g ALA (n-3)
Light Cream, conventional, grain-fed cows
0.5g LA (n-6)
0.3g ALA (n-3)
Sour Cream, conventional
0.4g LA (n-6)
0.3g ALA (n-3)
Milk, whole, conventional
0.1g LA (n-6)
0.1g ALA (n-3)
Yogurt, plain, whole milk, conventional
0.1g LA (n-6)
0.1g ALA (n-3)
Egg Yolks, conventional (100g = approximately 4 yolks)
2.6g LA (n-6)
0.05g ALA (n-3)
Egg Yolks, pastured or flaxseed included in diet
4.2g LA (n-6)
2.1g ALA (n-3)
Butter, conventional
2.73g LA (n-6)
0.32g ALA (n-3)
Butter, grass-fed organic
1.8g LA (n-6)
1.2g ALA (n-3)
Meats & Game
Elk
0.343g (n-6)
0.056g (n-3)
Bison
0.156g (n-6)
0.026g (n-3)
Beef, grass-fed
0.139g (n-6)
0.052g (n-3)
Beef, grain-fed, conventional
0.275g (n-6)
0.016g (n-3)
UPDATE - October 5, 2006
Venison, roast, cooked, braised (approximate levels)
0.13g (n-6)
0.06g (n-3)
Sources:
Medeiro, L.C. 2002. Nutritional content of game meat. B-920R. College of Agriculture, University of WyomingUSDA Nutrient Database
Asia Pac J Clin Nutr. 2006;15(1):21-9; Effect of feeding systems on omega-3 fatty acids, conjugated linoleic acid and trans fatty acids in Australian beef cuts: potential impact on human health
Lipids. 2005 Feb;40(2):191-202; A study on the causes for the elevated n-3 fatty acids in cows' milk of alpine origin
Asia Pac J Clin Nutr. 2003;12 Suppl:S38; Feeding regimes affect fatty acid composition in Australian beef cattle
J Nutr Health Aging. 2005 Jul-Aug;9(4):232-42; Where to find omega-3 fatty acids and how feeding animals with diet enriched in omega-3 fatty acids to increase nutritional value of derived products for human: what is actually useful?
Poult Sci. 2000 Jul;79(7):971-4; Enriched eggs as a source of N-3 polyunsaturated fatty acids for humans
Omega-3 Oils - A Practical Guide, Donald Rudin, MD, Clara Felix
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