Low-Carb Diet Study: But Wait, There's More!

Sometimes, even after you think you're done with crunching numbers in a study, the data somehow manages to keep mulling around in your head, teasing you to come back and take another look, quietly nagging at the back of your brain that there is something else, something important, go back and look again.

After reviewing the recently published Low-Carbohydrate-Diet Score and the Risk of Coronary Heart Disease in Women in the November issue of the New England Journal of Medicine, I posted Spinning Low-Carbohydrate Diet Study Data to highlight the headlines that claimed a low-carbohydrate diet rich with plant-based fats and protein had no basis in the data. If you read that article, you may recall I noted the finding of reduced risk was in the context of a dietary pattern where the lowest intake of carbohydrate was 202g each day compared with the highest of 242g each day. Not exactly low in carbohydrate and not exactly a remarkable difference in intake between the lowest and highest intake groups.

As I noted, in the context of an intake range of 202g to 240g carbohydrate, when subjects are consuming similar intake of red meat, chicken, fish - a higher consumption of nuts, coffee, saturated fat and whole grains with less fruits and vegetables may provide a benefit in the context of such a dietary pattern higher in carbohydrate.

But, at the time, it seems I missed something even more important than these very subtle differences between the groups. After my brain was insisting I return to the data, I went back, and something important (at least I think it's important) popped out - there was something remarkably different between the groups, more important than the differenece in consumption of nuts, red meat, coffee, alcohol, fruits and vegetables - the group consuming 202g of carbohydrate, the one with the reduced risk of cardiovascular disease, appears to have consumed enough polyunsaturated fatty acids (PUFA) to meet essential fatty acid (EFA) requirements; the group consuming 242g of carbohydrate each day didn't come close.

Intrigued?

I was!

So I went to the Institute of Medicine documents I have on file to double-check my memory about the level of intakes considered absolute minimum requirements for a female adult. Setting aside any arguement about exact ratios of omega fatty acids and any arguement of needing more omega-3 in the diet and less omega-6, sure enough, the IOM document includes a requirement that the group with reduced risk potentially met. Females, aged 31-70+, require between 0.6-1.2% of daily calories from omega-3 fatty acids and between 5-10% of daily calories from omega-6 fatty acids; with an absolute minimum requirement (regardless of calorie intake) of 1.1g of omega-3 and 11g-12g of omega-6 (females aged 31-70+); a absolute minimum of 12.1g-13.1g of essential fatty acids each day.

Essential fatty acids are found only in polyunsaturated fats, so to meet requirements one would have to consume more than the minimum requirement of polyunsaturated fats since not all polyunsaturated fats are essential fatty acids.

The group consuming 242g of carbohydrate each day only had 4.4% of their daily calories from PUFA - below the minimum requirement of 5.6% just for EFA from polyunsaturated fats. Taking it one step further, the 4.4% of calories worked out to just 8.5g of polyunsaturated fats each day - well below the minimum 12.1g-13.1g for EFA from polyunsaturated fats.

Compare that to the group with the 30% reduction in risk for cardiovascular disease - the group consuming 202g of carbohydrate - their diet included 7.4% of calories from PUFA, enough to meet the target intake of 5.6%. Taking it one step further, the 7.4% of calories each day worked out to 14.6g of polyunsaturated fats each day - enough to meet the 12.1g-13.1g minimum for EFA from polyunsaturated fats.

Big difference, isn't it?

In fact, if we look at each analysis - the total calorie analysis, with statistically insignificant differences between groups, they had minor differences between them for PUFA intake in absolute grams - 10.7g in the highest carbohydrate intake compared to 12g in the lowest carbohydrate intake; the animal calorie analysis showed 11.5g in the highest carbohydrate group compared to 10.3g in the lowest carbohydrate group.

The group with the real difference in PUFA intake was the plant-based calorie analysis, within this analysis the group with the lowest risk consumed much more PUFA - enough to theoretically meet essential fatty acid requirements when compared to the group at the other end of the spectrum whom did not consume enough to even come close to meeting requirements.

What increased PUFA intake in the group with reduced risk? That question leads back to the consumption of nuts, the one food the group ate significantly more quantity of. Nuts have repeatedly been assoicated with a reduced risk of heart disease and in this study, it seems they provided the boost to essential fatty acids that are necessary for overall good health.

Your People Live Only Upon Cod...

Thank you to SquareCube over at the Active Low-Carber Forum for this gem!

"Your People Live Only Upon Cod": An Algonquian Response to European Claims of Cultural Superiority

Now tell me this one little thing, if thou hast any sense: Which of these two is the wisest and happiest—he who labours without ceasing and only obtains, and that with great trouble, enough to live on, or he who rests in comfort and finds all that he needs in the pleasure of hunting and fishing? It is true, that we have not always had the use of bread and of wine which your France produces; but, in fact, before the arrival of the French in these parts, did not the Gaspesians live much longer than now? And if we have not any longer among us any of those old men of a hundred and thirty to forty years, it is only because we are gradually adopting your manner of living, for experience is making it very plain that those of us live longest who, despising your bread, your wine, and your brandy, are content with their natural food of beaver, of moose, of waterfowl, and fish, in accord with the custom of our ancestors and of all the Gaspesian nation. Learn now, my brother, once for all, because I must open to thee my heart: there is no Indian who does not consider himself infinitely more happy and more powerful than the French.

Source: William F. Ganong, trans. and ed., New Relation of Gaspesia, with the Customs and Religion of the Gaspesian Indians,by Chrestien LeClerq (Toronto: Champlain Society, 1910), 103–06

Do ya feel lucky?

...Well, do ya punk?

So much for "first, do no harm"

Just go read the article!

AHA: Industry Needs to Be Consulted Before Banning Trans-Fats

Oh, you're going to just love this one...

The AHA made clear their position on the proposed ban on trans-fats by New York City when Robert Eckle, President of the AHA, said the sudden removal of trans-fatty acids from restaurants is not a practical solution, telling heartwire that many individuals, from "field to mouth," are involved in the process and need to be consulted. He said the ban is unrealistic and unfairly punitive to the food and restaurant industry.

Say what? Those who make industrial trans-fatty acids need to be consulted?

Puh-leez!

But what can we expect from an organization that published the No Fad Diet, a book that recommends consumption of copious amounts of trans-fats as part of a heart-healthy diet?

Spinning Low-Carbohydrate Diet Study Data

The last two days have brought us headlines trumpting the long-term finding that low-carbohydrate diets do not increase the risk of heart disease:

• Low-Carb Diet Doesn't Up Heart Risk
• Study finds low-carb diets OK for heart
• Low-Carb Diet Can Be Heart-Healthy

These and other headlines were reporting the findings published yesterday in the New England Journal of Medicine in Low-Carbohydrate-Diet Score and the Risk of Coronary Heart Disease in Women. In this paper, researchers from Harvard School of Public Health and UCLA analyzed the Nurses' Health Study data, with more than 82,000 subjects over a period of twenty years with a low-carbohydrate diet score. The score was based on percentage of calories from carbohydrate, fat and protein.

As is almost always the case, what we're reading in the media reports isn't exactly what was published in the data.

For example, the Chicago Tribune reported "those who ate a low-carb diet but got more of their protein and fat from vegetables rather than animal sources cut their heart disease risk by 30 percent on average, compared with those who ate more animal fats."

Forbes reported "Heart risk was also 30 percent lower for participants who got their protein and fat from vegetables rather than from meat."

The Baltimore Sun reported "In a separate analysis, researchers divided the women based on their consumption of vegetable fat, such as olive oil. Women who derived the highest percentage of calories from vegetable fat had 30 percent lower risk of heart disease than those who ate a higher proportion of animal fats."

The various news accounts leave readers with the impression that the finding of reduced risk from vegetable fats and proteins was in the context of a low-carbohydrate diet. Surprise - it wasn't. Let's step back for a moment and take a look at the methods of analysis in the study so you can understand why the various media reports are disingenous and inaccurate.

To review the potential risk or benefit of a low-carbohydrate dietary pattern, the researchers devised a scoring system for determining whom amongst the Nurses' Health Study consumed a low-carbohydrate diet. Based on total carbohydrate, total fat and total protein, the reseachers found that 3,693 subjects consumed about 37% of their daily calories from carbohydrate. In absolute grams each day, this worked out to be 139g a day, with the mean intake of 116.7g. This was compared with the highest consumption of 267g each day, with a mean intake of 234.4g.

As the researchers noted in their full-text, this level was "similar to that consumed by participants in the clinical trials of low-carbohydrate diets." It was not very low-carbohydrate, but similar to something like Atkins maintenance or the Zone. After conducting a multivariate analysis (that is accounting for confounding variables like smoking, BMI, hormone replacement therapy, etc.) they found those consuming the low-carbohydrate dietary pattern had a reduced risk of cardiovascular disease, with a 6% reduction in risk. However, this was not statistically significant as the range of risk in the confidence interval crossed the "1" - it ranged from 0.76-1.18.

The finding is however significant in this sense - for years we've been warned that a low-carbohydrate diet might increase risk of cardiovascular disease. This study shows us that over a long period of time - twenty years - it does not increase risk, and even reduces risk slightly. A key piece of data not discussed in the media or even the paper - the number of individuals who followed such a dietary pattern was very small - 4.4% of all subjects from the Nurses' Health Study. I'll get to why this is important in a moment - let's look at what the researchers did next in their analysis.

Using the same scoring system, the researchers now wanted to know about risk based on consumption of animal fats and protein. Using the scoring system with these macronutrients as the primary focus, they again grouped subjects into ten deciles - this time based on those with the highest consumption of animal fats and protein examined. Interestingly, those with the highest consumption of animal fats and protein again consumed the least carbohydrate - this time an average 128g per day. This was compared with the highest carbohydrate consumption group eating an average of 264g each day. And, again, using the multivariate analysis, an identical reduction of risk was found - 6%; with the range being 0.74-1.19; statistically insignificant when compared with the lowest intake of animal fats and protein. Noteworthy here - even less subjects consumed this dietary pattern - just 3.5% of participants in the study.

Both of these analysis were low in carbohydrate, but the researchers had one more question to ask - what about vegetable fats and protein? Once again they scored subjects, this time based on consumption of plant based calories for each macronutrient. And, AHA!, they found statistical significance! Those who consumed higher levels of plant based fats and proteins had a statistically significant reduction in cardiovascular risk.

Too bad it wasn't a low-carbohydrate diet. In this analysis, the lowest group intake of carbohydrate was 202g each day, compared with 242g each day in the highest intake group. There are two problems with this - one, the difference between the highest intake of carbohydrate and the lowest intake is minor, and two, in absolute grams each day, both the highest intake and lowest intake consumed almost identical animal fat and protein. Add to this, the lowest carbohydrate group now accounted for 9.3% of the subjects and it's easier to understand why this particular finding has nothing to do with low-carbohydrate diets - both of the previous analysis found less than 5% consuming a low-carbohydrate dietary pattern and here, we now have a larger population, consuming a much greater intake of carbohydrate, being used to conclude vegetable fats and protein are protective on a low-carbohydrate diet.

Nonsense!

The dietary pattern in the third analysis had one major difference in foods eaten...and it wasn't red meat or any animal food for that matter....it was nuts.

The group that was found to have a reduced risk ate four times as many nuts each week - 2.8 servings a week compared with less than 1 (0.7 servings per week). This led to something else being different - magnesium intake. The group consuming more nuts also consumed much more magnesium - 320mg each day compared to just 284mg a day.

The group with a reduced risk also had 29% taking a multivitamin compared with 23% in the group at the extreme other end. One last interesting finding with this group - they ate less fruit and vegetable than the other groups, consumed more coffee and, gasp!, consumed more saturated fat!

So, we find the analysis that claims that vegetable fats and protein are protective in a low-carbohydrate diet are not based on the data here - the dietary pattern was not low-carbohydrate, the group was not shunning animal foods (as implied), and they were not eating more fruits and vegetables (as implied).

The researchers did indeed find there was no risk to following a low-carbohydrate diet in the long-term; they even found that high intakes of animal fats and protein wasn't going to increase your risk of cardiovascular disease. What they didn't find is that vegetable fats and protein are protective in the context of a low-carbohydrate diet.

Instead they found, in the context of an intake range of 202g to 240g carbohydrate, when subjects are consuming similar intake of red meat, chicken, fish - a higher consumption of nuts, coffee, saturated fat and whole grains with less fruits and vegetables may provide a benefit in the context of such a dietary pattern higher in carbohydrate. Just don't expect them to tell you that - instead they'll continue to perpetuate the myth that animal foods and saturated fat is detrimental to your health.

Take home message here - the data is clear that if you're following a low-carbohydrate dietary pattern, a diet that is in the range of 100-130g per day - even one rich with animal foods, you do not have an increased risk of cardiovascular disease.

Since it's November, and it's National Diabetes Month, I'm going to ask - when will the American Diabetes Association start to seriously consider drafting a clinical guideline for those at risk for or diagnosed with diabetes to have the option of trying a low-carbohydrate diet to control their blood sugars?

A Face of Diabetes: Alan, Committed to Control

Back in January I wrote about how Diabetics Must Demand Accontability from the ADA and put it bluntly - "Rather than admit their dietary recommendations are contributing to the progressive degeneration of those with diabetes, they remain staunch that this type of “treatment” is the best we have."

When the ADA updated their Medical Nutrition Therapy (MNT) in August, I took the position the ADA has Become Irrelevant and wrote "After decades of research time, millions of dollars, and billions of manhours - the ADA has not only failed find a solution to prevent diabetes, it is also currently unable to curtail the epidemic of diabetes.

While admitting the "current-day management has failed to achieve and maintain the glycemic levels most likely to provide optimal health care status for people with diabetes," they continue down the very same path that leads to slow, insidious progression of the disease."

I followed up with Should we Debate Diet for Diabetes? and included "on the one hand we have the ADA acknowledging its dietary advice is worthless; on the other we have the ADA refusing to adopt, even cautiously, a dietary recommendation shown to improve blood sugars, insulin and HbA1C, and reduce risk markers for diabetic complications - a low-carb diet."

Earlier this week I learned of a gentleman in Australia, Alan, who has type II diabetes and who blogs at Type II Diabetes - A Personal Journey. His blog is fairly new and provides insight about his experience learning how to manage his diabetes. A post made on November 2, 2006 caught my attention - Diabetes Authorities and Diet. In that post he includes a letter he sent a couple of years ago to the Editor of Conquest: Diabetes Australia (a quarterly magazine).

Rather than summarize what he wrote, here is the post in it's entirety (with permission):

--------

What follows is a copy of a letter I wrote a couple of years ago to the Editor of Conquest, the Diabetes Australia (DA) quarterly magazine. Since then, nothing has changed - so I'll repeat it as sent. Because my opinion hasn't changed either. For accuracy, I will note that I have added 1000mg metformin daily since writing the letter, so I can no longer claim to "take no diabetes medications". But that doesn't change the thrust of my argument.

To be clear, I think that both DA and the American Diabetes Association are marvellous, worthy organisations doing sterling work for diabetics in both countries. My only disagreement is specifically to do with their dietary and testing guidelines. The dietary advice and guidelines promoted by DA is effectively a rubber-stamp of that issued by the ADA; so the same comments apply to both.

I never received a reply.

I am eternally grateful for the work the pioneers at Diabetes Australia did in helping us get the NDSS and the support system that we now have. The organisation continues to do a great job. But I have a basic difficulty with the logic of the dietary advice recommended by your dieticians.

I see their advice like this:

1. Dieticians advise high complex carbohydrate consumption, apparently for heart, kidney and vascular health;

2. High complex carbohydrate consumption causes high blood glucose levels;

3. High blood glucose levels cause diabetic complications such as retinopathy, neuropathy, nephropathy and heart disease;

4. DA dieticians therefore recommend balancing the high complex carbohydrate consumption with medication or insulin to control blood glucose levels.

This advice appears to be in line with the recommendations of overseas organisations such as the American Diabetes Association (ADA).

Specific examples can be found on the DA web-site at http://www.diabetesaustralia.com.au/multilingualdiabetes/healthpros/FoodNut/healthy.htm

or the ADA web-site at
http://www.diabetes.org/nutrition-and-recipes/nutrition/starches.jsp

My difficulty in understanding this is because no-one seems to be investigating the alternative approaches. I don't mean herbs and supplements, just a better diet for diabetics, together with exercise, to enable minimal medication.

To me, the most obvious alternative is to search for a diet for the diabetic which provides adequate nutrition for good health but does not cause high blood glucose levels. If such a diet is possible it would minimise the need for medication, particularly for type 2, with side benefits for overall health and health costs. I can attest that it is possible; I've done it, as have many others. However, when diabetics write to give examples, such as K ...... in the Autumn issue, they are dismissed and told that their improvement must be because of exercise, or weight loss, or some other factor.

The method I followed, as a type 2, was simple. I started with a standard, sensible diet to lose weight. Then, as I followed that diet, I tested everything I ate one hour and two hours after I ate it. If I consistently found that something led to high blood glucose, I changed it. Sometimes I changed the food, sometimes the quantity, sometimes the timing, but always the aim was to minimise "spikes". Gradually I found I was eating significantly less carbohydrates, a little more protein and a little more "good" oils. And I did a little "lazy man's" exercise along the way. I also gradually reduced the high level of initial testing as results became predictable.

After attaining a degree of control over my blood glucose, I now progressively review my diet to ensure there are no missing nutritional requirements and to further improve lipids etc. At diagnosis in 2002 my HbA1c was 8.2, now it's 5.9 and I take no diabetes medications. It's a long time since I've seen a "spike" over 8, rarely over 7.5. The improvements continued long after I reached my target weight. And my heart, blood pressure, lipids, kidneys and so on are also in good shape.

Why do your dieticians continue to promote high carbohydrate consumption? What is it I'm missing, apart from complications?

Cheers, Alan, T2, Australia.
Everything in Moderation - Except Laughter

Can Diabetics Have Normal Blood Sugars with Diet Alone?

Yesterday Dr. Mike Eades, in his post Saturated Fat info at ASBP, mentioned the presentation given by Dr. Eric Westman - Low-GI, Low-Carbohydrate Diets in Diabetes - at the American Society of Bariatric Physicians meeting last week. I was unable to attend the meeting, but Dr. Westman provided me a copy of the presentation since it's a topic I'd like to discuss here today.

Early in his presentation, Dr. Westman highlights the American Diabetes Association (ADA) goals of Medical Nutrition Therapy:

• Attain and maintain optimal metabolic outcomes including:
• Blood glucose levels in the normal range or as close to normal as safely possible to prevent or reduce the risk for complications of diabetes
• A lipid and lipoprotein profile that reduces the risk for macrovascular disease
• Blood pressure levels that reduce the risk for vascular disease
• Prevent and treat the chronic complications of diabetes
• Improve health through healthy food choices and physical activity
• Address individual nutritional needs taking into consideration personal and cultural preferences and lifestyle

This provided a nice segway into the comparison of dietary trial outcomes where carbohydrate included was measured by glycemic index and/or load or total carbohydrate in the diet.

Beginning with evidence dating back to 1982, he highlighted that carbohydrate directly leads to an increase in post-prandial glucose and insulin response; included recent data showing glycemic index is a major factor, but with more fat included the response is reduced in meals; and then followed-up with data from 2003 that clearly found glucose and insulin response was most favorable when subjects consumed a low-carbohydrate diet.

One of the most interesting slides was the one that went way back - to the 1920's - to review how diabetes was treated with diet alone before insulin! Citing three different publications, he showed that the dietary recommendation back then was clearly low-carbohydrate; with the recommendation for someone weighing 60kg (132-pounds) being 1795-calories with 10g carbohydrate (40 calories), 75g protein (300 calories), 150g of fat (1350 calories) and 15g of alcohol (105 calories). Imagine that, a low-carb diet was the treatment way back before we had any pharmaceuticals to offer.

Fast forward to recently published data and he presents a dozen studies that convincingly make the case that it isn't just the quality of the carbohydrate (GI-GL), but the reduction in total carbohydrate in the diet that offers the most significant improvements for those with diabetes.

Two case studies, in fact, are compelling because they not only provide data showing significant improvements, they show subjects HbA1c reduced to below 6% - into the normal range! [While below 6% is "normal," later this month I'll include an article about what levels are optimal to reduce the risk of cardiovascular disease and why]

The first highlighted in the presentation was published in December 2003 in journal Metabolic Syndrome and Related Disorders, The Effects of a Low-Carbohydrate Regimen on Glycemic Control and Serum Lipids in Diabetes Mellitus. The case study involved a "chart review...of 30 patients who self-reported the consumption of 30 g of carbohydrate daily, followed a strict insulin regimen, monitored blood glucose levels at least four times daily, and had follow-up clinical visits or phone calls with their physician. For both type I and type II diabetics, there were significant improvements in glycemic control and mean fasting lipid profiles at follow-up."

How significant?

HbA1c levels dropped, over an average of 21.4 months, from 7.9 to 5.7 - much lower than the ADA target of 7 and the International Diabetes Federation (IDF) target of 6.5.

Additionally, significant improvements were reported for:

• weight (average 5kg weight loss)
• LDL (decreased from 155.4 to 129.7)
• Triglycerides (decreased from 106.8 to 73.6)
• HDL (increased from 50.4 to 73.6) and
• Total Cholesterol-to-HDL ratio (decreased from 4.99 to 3.42).

Non-significant changes included a reduction in total cholesterol from 229 to 222, and a reduction in the use of insulin from 32 units to 25 units on average.

As the researchers noted, "A carbohydrate-restricted regimen improved glycemic control and lipid profiles in selected motivated patients."

In the he second case study, Clinical Experience of a Carbohydrate-Restricted Diet: Effect on Diabetes Mellitus, published in the September 2003 issue of the same journal, researchers undertook a a similar review of patient charts over a period of 18-months, and again, significant changes were found for triglycerides and HbA1c.

In this study, HbA1c was reduced from 10 to 5.9 over the 18-months of follow-up - again within the normal range and well below the targets set by the ADA and the IDF.

Most compelling were some of the unpublished data from Dr. Mary Vernon's practice that was presented to show the dramatic effect reducing carbohydrates in the diet has on HbA1c - the improvement is not only almost immediate, it is striking how quickly HbA1c falls below the ADA and IDF targets!

• Male, 50, 26-months low-carb, HbA1c 7.0 ---> 5.3
• Female, 58, 8-months low-carb, HbA1c 6.4 ---> 5.5
• Female, 49, 12-months low-carb, HbA1c 6.0 ---> 5.1
• Female, 39, 3-months low-carb, HbA1c 16.8 ---> 5.3
• Male, 44, 4-months low-carb, HbA1c 8.7 ---> 4.8
• Female, 69, 5-months low-carb, HbA1c 8.1 ---> 5.4
• Female, 33, 15-months low-carb, HbA1c 10.9 ---> 4.8
• Male, 50, 26-months low-carb, HbA1c 9.0 ---> 5.3
• Female, 36, 18-months low-carb, HbA1c 9.2 ---> 5.5

Now to be fair and include all the relevant data, it must be said that the dietary approach does not reduce HbA1c below the targets for everyone. Of the thirteen profiles highlighted, four patients did have significant improvements, but did not see an improvement to below 6.0 and it is noteworthy that these four individuals had the highest HbA1c levels of the subjects included:

• Male, 59, 16-months low-carb, HbA1c 12.0 ---> 7.4
• Female, 49, 12-months low-carb, HbA1c 12.5 ---> 7.5
• Male, 56, 2-months low-carb, HbA1c 12.0 ---> 6.8
• Female, 35, 3-months low-carb, HbA1c 11.3 ---> 6.3

In comparing low-carbohydrate trials to conventional studies, the data is powerful, especially for reduction of HbA1c:

• DCCT trail, conventional approach, HbA1c to 8.9
• DCCT trial, intensive treatment, HbA1c to 7.1
• Hays, 100g carbohydrate daily, HbA1c to 6.9
• Bernstein, 30g carbohydrate daily, HbA1c to 5.7
• Vernon, 20g carbohydrate daily, HbA1c to 5.9
• Yancy, 42g carbohydrate daily, HbA1c to 6.3 (most significant to 5.8 in those who discontinued medication and attained glycemic control by diet alone)

At the end of the day, Dr. Westman nailed it - a low glycemic index diet may be politically correct, but it's the low-carbohydrate diet that offers the best glycemic control and improvements in data from studies of subjects with diabetes.

As he noted, low-carbohydrate diets are low glycemic index diets. The real difference is that a low glycemic index diet may still include up to 50% of calories from carbohydrate whereas a low-carbohydrate diet specifically limits the consumption of total carbohydrates in a day with careful attention to not only the total carbohydrate, but the quality of the source of carbohydrate.

As the case studies presented clearly show, attaining glycemic control is possible when the diet is modified to restrict carbohydrate intake. Significant improvements are found in not only the HbA1c levels, but also triglycerides, HDL, LDL and weight.

It's November and it's National Diabetes Month - isn't it time we started to ask why the ADA refuses to even offer patients the option to try a low-carbohydrate diet to control their blood sugars?

November is National Diabetes Month

It's November and that means it's National Diabetes Month!

This year my blog is going to focus on diabetes throughout the month - I'll highlight issues, evidence and resources for those at risk for or diagnosed with diabetes, and also introduce you to a number of individuals who have taken charge of their health and are effectively controlling blood sugars through various approaches.

We often hear and read about the "inevitable" complications of diabetes - throughout the month I wish to bring hope, highlight approaches that may keep those complications away, and feature individuals who are living examples of those not content with simply "good enough" but whom are committed to excellence in controlling their diabetes. It is my hope these individuals will inspire and motivate readers to learn more about why controlling blood sugars is critically important and how to effectively educate yourself about how to regain control.

As you'll learn throughout the month, it isn't always easy, it isn't always fun, and it isn't always by the ADA guidelines. That's the beauty of getting to know these folks - they searched, educated themselves, tweaked and still continously modify as they integrate various approaches into their daily lives that work for them as individuals. While those diagnosed with diabetes share many common health issues, diabetes is still an individual disease that one must tackle like any other challenge in life - by finding what works for you as an individual!

I'll also highlight recent developments in the research, address various issues that are often on the minds of those with diabetes, and present various resources to help my readers continue learning more!

November is National Diabetes Month - let's take this opportunity to learn and grow in our understanding of what is quickly becoming a national health crisis so we can reverse the current trends and take back our health as a nation!

A Sticky Question about Fruit in the Diet

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!

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!

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.

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:

• 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!

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!

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...

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.

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.

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!

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!

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...

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:

• 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!

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.

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.

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