- 2 quarts apple cider
- 1 cup Pure Vermont Maple Syrup
- 1 stick cinnamon
- A few whole cloves
- Lemon slices, cut in half, for garnish
Wednesday, December 30, 2009
Tuesday, December 29, 2009
How is it that most peoples' body fat mass stays relatively stable over long periods of time, when an imbalance of as little as 5% of calories should lead to rapid changes in weight? Is it because we do complicated calculations in our heads every day, factoring in basal metabolic rate and exercise, to make sure our energy intake precisely matches expenditure? Of course not. We're gifted with a sophisticated system of hormones and brain regions that do the calculations for us unconsciously*.
When it's working properly, this system precisely matches energy intake to expenditure, ensuring a stable and healthy fat mass. It does this by controlling food seeking behaviors, feelings of fullness and even energy expenditure by heat production and physical movements. If you eat a little bit more than usual at a meal, a properly functioning system will say "let's eat a little bit less next time, and also burn some of it off." This is why animals in their natural habitat are nearly always at an appropriate weight, barring starvation. The only time wild animals are overweight enough to compromise maximum physical performance is when it serves an important purpose, such as preparing for hibernation.
I recently came across a classic study that illustrates these principles nicely in humans, titled "Metabolic Response to Experimental Overfeeding in Lean and Overweight Healthy Volunteers", by Dr. Erik O. Diaz and colleagues (1). They overfed lean and modestly overweight volunteers 50% more calories than they naturally consume, under controlled conditions where the investigators could be confident of food intake. Macronutrient composition was 12-42-46 % protein-fat-carbohydrate.
After 6 weeks of massive overfeeding, both lean and overweight subjects gained an average of 10 lb (4.6 kg) of fat mass and 6.6 lb (3 kg) of lean mass. Consistent with what one would expect if the body were trying to burn off excess calories and return to baseline fat mass, the metabolic rate and body heat production of the subjects increased.
Following overfeeding, subjects were allowed to eat however much they wanted for 6 weeks. Both lean and overweight volunteers promptly lost 6.2 of the 10 lb they had gained in fat mass (61% of fat gained), and 1.5 of the 6.6 lb they had gained in lean mass (23%). Here is a graph showing changes in fat mass for each individual that completed the study:
We don't know if they would have lost the remaining fat mass in the following weeks because they were only followed for 6 weeks after overfeeding, although it did appear that they were reaching a plateau slightly above their original body weight. Thus, nearly all subjects "defended" their original body fat mass irrespective of their starting point. Underfeeding studies have shown the same phenomenon: whether lean or overweight, people tend to return to their original fat mass after underfeeding is over. Again, this supports the idea that the body has a body fat mass "set point" that it attempts to defend against changes in either direction. It's one of many systems in the body that attempt to maintain homeostasis.
OK, so why do we care?
We care because this has some very important implications for human obesity. With such a powerful system in place to keep body fat mass in a narrow range, a major departure from that range implies that the system isn't functioning correctly. In other words, obesity has to result from a defect in the system that regulates body fat, because a properly functioning system would not have allowed that degree of fat gain in the first place.
So yes, we are gaining weight because we eat too many calories relative to energy expended. But why are we eating too many calories? Because the system that should be defending a low fat mass is now defending a high fat mass. Therefore, the solution is not simply to restrict calories, or burn more calories through exercise, but to try to "reset" the system that decides what fat mass to defend. Restricting calories isn't necessarily a good solution because the body will attempt to defend its setpoint, whether high or low, by increasing hunger and decreasing its metabolic rate. That's why low-calorie diets, and most diets in general, typically fail in the long term. It's miserable to fight hunger every day.
This raises two questions:
- What caused the system to defend a high fat mass?
- Is it possible to reset the fat mass setpoint, and how would one go about it?
* The hormone leptin and the hypothalamus are the ringleaders, although there are many other elements involved, such as numerous gut-derived peptides, insulin, and a number of other brain regions.
Saturday, December 26, 2009
The facts and findings have been confirmed and the evidence supports the scientists' and doctors' contention that disease is a result of the progressive degeneration of the body's own natural ability to heal, protect and maintain its own health at optimum levels.
Through general study and analysis as to why the information available through the scientific health community had not been made readily available to the medical health institutes and universities became quite apparent.
Although many of the discoveries were reported and published to the professional medical journals such as J.A.M.A. etc these were never highly promoted through university and curriculum study. There has been no vehicle in place to promote or provide the findings to the public.
As the health care crisis increses in severety here in the United States, we see the need for a call to action. The ASH program is a solution for millions that are suffering. The program invites Medical professionals, health care workers and families to review the material. A website has been developed to provide audios, lectures and resources available via the internet to help medical professionals determine what level of participation would best serve their patients and how to best integrate the ASH program into their current service model.
A portion of the facts and findings will be posted here on the Scientific Health Journal to help anyone further their understanding in how to best help themselves and others in applying this life saving knowledge.
No one need suffer with pain and early death. The answers are here for anyone. A great place to start is to go back and review what worked before. A very easy to read publication is available free:
"Conclusions of Dr. Frederick Klenner M.D."
We will be releasing the findings here as we also roll out the program so please be patient. Should you have any questions, please feel free to contact us at: www.AdvancedScientificHealth.net Welcome 2010 ~ We Are Ready !
Friday, December 25, 2009
In this study, they fed four groups of rabbits different diets:
- Regular low-fat rabbit chow
- Regular low-fat rabbit chow plus 0.5 g cholesterol per day
- High-fat diet with 30% calories as coconut oil (saturated) and no added cholesterol
- High-fat diet with 30% calories as sunflower oil (polyunsaturated) and no added cholesterol
Total cholesterol was also the same between all groups except the cholesterol-fed group. TBARS, a measure of lipid oxidation in the blood, was elevated in the cholesterol and sunflower oil groups but not in the chow or coconut groups. Oxidation of blood lipids is one of the major factors in atherosclerosis, the vascular disease that narrows arteries and increases the risk of having a heart attack. Serum vitamin C was lower in the cholesterol-fed groups but not the others.
This supports the idea that saturated fat does not inherently increase LDL, and in fact in most animals it does not. This appears to be the case in humans as well, where long-term trials have shown no difference in LDL between people eating more saturated fat and people eating less, on timescales of one year or more (some short trials show a modest LDL-raising effect, but even this appears to be due to an increase in particle size rather than particle number). Since these trials represent the average of many people, they may hide some individual variability: it may actually increase LDL in some people and decrease it in others.
Thursday, December 24, 2009
In adults, growth hormone deficiency is associated with: decreased calcium retention and osteoporosis, loss of muscle mass, increased fat deposition, decreased protein synthesis, and immunodeficiency. In children, growth hormone deficiency is associated with stunted growth.
Levels of growth hormones decline with age, and their decrease is believed to contribute to the aging process. Abdominal obesity is associated with low levels of growth hormone, and is also associated with the onset of the metabolic syndrome, a precursor of diabetes and cardiovascular disease.
While there are many treatments in the market that include exogenous administration of growth hormones (e.g., through injection), there are several natural ways in which growth hormone levels can be increased. These natural ways can often lead to more effective and sustainable results than prescription drugs.
For example, fasting stimulates the natural production of growth hormone. So does vigorous exercise, particularly resistance exercise with a strong anaerobic component (not cardio though). And, to the surprise of many people, deep sleep stimulates the natural production of growth hormone, perhaps more than anything else. (Although only once every 24 hours; sleeping all day does not seem to work.)
In fact, during a 24-hour period, growth hormone typically varies in pulses, or cycles. The pulses are somewhat uniformly distributed during the day, with a peak occurring at night. The graph below (source: Fleck & Kraemer, 2004) plots the typical variation of growth hormone during a 12-hour period, including the deep sleep period.
As you can see, growth hormone peaks during deep sleep; which is achieved a few hours after one goes to bed, and not too long before one wakes up.
By the way, if you want to know more about human physiology and metabolism, forget about popular diet and exercise books. Next to peer-reviewed academic articles (which are often hard to read), the best sources are college textbooks used in courses on physical education, nutrition, endocrinology, and related topics. The book from which the graph above was taken (Fleck & Kraemer, 2004), is a superb example of that.
Fleck, S.J., & Kraemer, W.J. (2004). Designing resistance training programs. Champaign, IL: Human Kinetics.
Wednesday, December 23, 2009
An excellent post by Michael Eades clarifies a number of issues with the study, including what one could argue is the study's main flaw. Apparently the study compared a half-hearted Atkins diet, with probably equally half-hearted Ornish and
I refer to the study's Atkins diet as half-hearted because it seems to rely on a daily consumption of between 120 and 180 grams of carbohydrates. This is unlikely to lead to ketosis, the cornerstone of the Atkins diet, where the body uses ketone bodies (made from dietary as well as body fat) as a source of energy.
As I see it, the main findings of the study were that the participants in the half-hearted Atkins diet, after a period of 4 weeks on the diet, and when compared with the participants in the other diets, had: (a) greater levels of total cholesterol and LDL cholesterol, with only a small improvement in their HDL cholesterol and triglycerides levels; and (b) greater levels of markers for inflammation (e.g., C-reactive protein).
The participants were young and healthy. Their average age was 30.6 years, and their average body mass index was 22.6. On average, their total cholesterol was 184.9 mg/dL, triglycerides were 78.1 mg/dL, LDL cholesterol was 107.2 mg/dL, and HDL cholesterol was 62.2 mg/dL. These are arguably fairly healthy numbers; although quite a few doctors might want to put most of these folks preventively on statins because of their LDL being greater than 100.
What I find interesting about this study, and consistent with both my own experience and also a theory that I have, is that it suggests that a low carb. diet has to really be low carb. in order to bring about the benefits that one normally sees as a result of a diet that induces ketosis. A diet with, say, > 150 g of refined grains per day, is not really a low carb. diet.
Again, in my experience, and that of many other people, a truly low carb. diet (very low in, if not devoid of, refined carbs and sugars), will lead to an impressive increase in HDL cholesterol (especially for those who have low HDL to start with), an equally impressive decrease in triglycerides, increased insulin sensitivity, and possibly a decrease in LDL.
However, a half-hearted Atkins diet may actually lead to elevated LDL (of the small-dense type), and more inflammation, just like this study suggests it does, without the benefits regarding HDL and trigs. The reason is that the still relatively high level of carbohydrate intake, especially if it comes in the form of refined carbs. and sugars, will lead to higher levels of insulin being secreted into the bloodstream. This will promote increased body fat deposition. The extra saturated fat being consumed will be turned into body fat, and not used as energy, starving the cells and leading to increased hunger.
A diet rich in saturated fat may indeed be bad when it is also a diet even moderately rich in insulin-boosting, easily digestible carbs. This may be one of the main reasons why there have been so many studies in the past showing a correlation between saturated fat consumption and heart disease; studies that typically did not control for carbohydrate consumption.
In a recent interview on the Livin' La Vida Low-Carb Blog, Dr. John Salerno goes into more detail regarding this issue, recommending a much more rigid adoption of the Atkins diet than many think is okay. (In fact, I often talk to people who think that if they cut a very high carb. intake in half - e.g., from 400 to 200 grams per day - replacing the carbs with fat, they will be halfway into a full blown Atkins diet.) Dr. Salerno has worked in the past with Dr. Atkins. He calls his diet the Silver Cloud Diet. I am not sure I agree with all that Dr. Salerno had to say, but his argument in favor of a diet very low in carbs. does make sense to me.
Finally, I think that it is dangerous to extrapolate the results of any study, no matter how comprehensive, to the population in general. Each individual is unique in terms of his or her genetic makeup and life history; the latter also influences metabolic patterns. (Even identical twins raised together may display different metabolic patterns, because of their different life histories.) So, while a low carb. diet may work well for a lot of people, it may have very negative effects on a few. Increases in inflammation markers and adverse effects on LDL cholesterol (especially when LDL is measured directly, accounting for particle numbers and sizes) are warning signs that any low carb. dieter should pay attention to.
Miller, M. et al. (2009). Comparative effects of three popular diets on lipids, endothelial function, and c-reactive protein during weight maintenance. Journal of the American Dietetic Association, 109, 713-717.
The Yamas and Niyamas, the first two branches of Patanjali's Eightfold Path from the Yoga Sutras, are very useful this time of year. Of particular interest are Ahimsa and Aparigraha from among the Yamas, and Santosha and Swadhyaya from the Niyamas.
Ahimsa - Non-Harming
Whether you are vegetarian or not, there is one being you can seek to refrain from harming all of the time: Yourself.
This applies to the choices you make about what you put into your body. Remember, most things are not going to harm you in moderation. The danger of this time of year is the quantity of food, alcohol, and sweets available - not to mention the additional social engagements involving eating. Plus, with less time to get everything done, more people skip their workouts - when this is the time we should be working out even more! Commit to keeping yourself healthy this entire holiday season and you will feel less stressed and have more energy to spread the joy.
Ahimsa also applies to negative self-talk. So don't beat yourself up if you can't do it all this season!
Aparigraha - When Enough's Enough
Sometimes, the toughest part of eating during the holidays is simply pushing away from the table. Aparigraha reminds us to listen carefully to our bodies and stop eating when we have eaten enough. Try to put your fork down between each bite of food and focus on chewing your food while you eat. If you are afraid of wasting food, or feel obliged to make excuses, ask for a doggy bag for leftovers to take home. Many home cooked or restaurant meals can be dinner and lunch the next day. Hostesses will be flattered if you say you're full, but perhaps could pack a few leftovers to take home? As long as you will eat them later, it isn't greedy to ask for doggy bags to save food from going to waste.
Santosha - Contentment
What's more important about the Holidays: the food or the company? Okay, so the truth is most people think it's a little bit of both. But just because you love holiday food, that doesn't mean you have to heap your plate to overflowing. If you practice contentment with the present moment, living in the "Now", you will be able to eat mindfully. Taste the smaller portions to their fullest, and truly savor each bite. Enjoy the sights, smells, sounds and the company that create the Holiday atmosphere as much as or perhaps even more than the food.
Swadhyaya - Save Room for Dessert
You know what your favorite holiday foods are. If you are certain beyond a shadow of a doubt that you will have a slice of Auntie Darlene's Black Forest Cake at the end of a meal, be aware of that throughout the meal. Eat only a bite of stuffing to appreciate the flavors, perhaps skip the mashed potatoes and gravy entirely. We all know how to make good decisions about eating, but we forget our sense of moderation in the melee of Holiday hubbub. Even if you choose to celebrate with merry abandon, please remember to be kind to yourself above all else.
Keep it fresh!
Tuesday, December 22, 2009
Elevated fasting insulin is a hallmark of the metabolic syndrome, the quintessential modern metabolic disorder that affects 24% of Americans (NHANES III). Dr. Lamarche and colleagues found that having an insulin level of 13 uIU/mL in Canada correlated with an 8-fold higher heart attack risk than a level of 9.3 uIU/mL (1; thanks to NephroPal for the reference). So right away, we can put our upper limit at 9.3 uIU/mL. The average insulin level in the U.S., according to the NHANES III survey, is 8.8 uIU/mL for men and 8.4 for women (2). Given the degree of metabolic dysfunction in this country, I think it's safe to say that the ideal level of fasting insulin is probably below 8.4 uIU/mL as well.
Let's dig deeper. What we really need is a healthy, non-industrial "negative control" group. Fortunately, Dr. Staffan Lindeberg and his team made detailed measurements of fasting insulin while they were visiting the isolated Melanesian island of Kitava (3). He compared his measurements to age-matched Swedish volunteers. In male and female Swedes, the average fasting insulin ranges from 4-11 uIU/mL, and increases with age. From age 60-74, the average insulin level is 7.3 uIU/mL.
In contrast, the range on Kitava is 3-6 uIU/mL, which does not increase with age. In the 60-74 age group, in both men and women, the average fasting insulin on Kitava is 3.5 uIU/mL. That's less than half the average level in Sweden and the U.S. Keep in mind that the Kitavans are lean and have an undetectable rate of heart attack and stroke.
Another example from the literature are the Shuar hunter-gatherers of the Amazon rainforest. Women in this group have an average fasting insulin concentration of 5.1 uIU/mL (4; no data was given for men).
I found a couple of studies from the early 1970s as well, indicating that African pygmies and San bushmen have rather high fasting insulin. Glucose tolerance was excellent in the pygmies and poor in the bushmen (5, 6, free full text). This may reflect differences in carbohydrate intake. San bushmen consume very little carbohydrate during certain seasons, and thus would likely have glucose intolerance during that period. There are three facts that make me doubt the insulin measurements in these older studies:
- It's hard to be sure that they didn't eat anything prior to the blood draw.
- From what I understand, insulin assays were variable and not standardized back then.
- In the San study, their fasting insulin was 1/3 lower than the Caucasian control group (10 vs. 15 uIU/mL). I doubt these active Caucasian researchers really had an average fasting insulin level of 15 uIU/mL. Both sets of measurements are probably too high.
We also have data from a controlled trial in healthy urban people eating a "paleolithic"-type diet. On a paleolithic diet designed to maintain body weight (calorie intake had to be increased substantially to prevent fat loss during the diet), fasting insulin dropped from an average of 7.2 to 2.9 uIU/mL in just 10 days. The variation in insulin level between individuals decreased 9-fold, and by the end, all participants were close to the average value of 2.9 uIU/mL. This shows that high fasting insulin is correctable in people who haven't yet been permanently damaged by the industrial diet and lifestyle. The study included men and women of European, African and Asian descent (7).
One final data point. My own fasting insulin, earlier this year, was 2.3 uIU/mL. I believe it reflects a good diet, regular exercise, sufficient sleep, a relatively healthy diet growing up, and the fact that I managed to come across the right information relatively young. It does not reflect: carbohydrate restriction, fat restriction, or saturated fat restriction. Neither does the low fasting insulin of healthy non-industrial cultures.
So what's the ideal fasting insulin level? My current feeling is that we can consider anything between 2 and 6 uIU/mL within our evolutionary template, although the lower half of that range may be preferable.
By Rik Ganderton, President and CEO
It has neither been the best of times nor the worst of times, to re-phrase a Charles Dickens line.
We have lived and worked through the greatest global recession in living memory, yet with this backdrop Rouge Valley has really found its footing as a patient-centred hospital relentlessly focused on improving the quality of care it delivers. We have dealt with many challenges in the last year and overcome them. Our staff, senior management team, physicians and volunteers have increasingly been working as a strong, cohesive team.
I will summarize some of our highlights of 2009 as successes, weaknesses, opportunities and threats to RVHS. As a reminder, we have all determined that our Vision is “to be the best at what we do.” And we have taken many strides towards that Vision this year.
Here are some of my thoughts on how Rouge Valley has fared in 2009.
We have had many, but here are a few top-of-mind ones.
• Our focus on quality yielded our hospital’s three-year accreditation. The surveyors found that our Strategic Plan-On-A-Page was among the best implemented and best known that they had seen and they spotlighted our Passport to Patient Safety training sessions as exemplary.
• The Central East Local Health Integration Network (CE LHIN) named our cardiac care program as a regional centre for the 401 corridor, recognizing years of ongoing patient care excellence.
• The opening of our new diagnostic imaging, fracture clinic and emergency department at Rouge Valley Ajax and Pickering (RVAP), which went live at 4 a.m. on Nov. 30, 2009, was a great success for us all and especially for our community. (See the photo of our first patient at this link.
• We are being recognized for our ongoing application of Lean management and methods by the CE LHIN and the broader industry. Some fine examples of Lean results by the Rouge Team include –
o Improved patient flow and discharge planning for patients at both of our hospital campuses.
o Faster turnaround times achieved for patients’ lab test results at both campuses.
o Shorter waits for our patients in emergency and shorter ambulance offload times at Rouge Valley Centenary (RVC).
• The new Birthing and Newborn Centre at RVC recently celebrated its first full year of delivering babies. Staff at the new centre have also led the way in implementing electronic documentation, which has improved the quality and accuracy of charting and improved processes for all staff using the system.
• We have received notification of first-year operating funding for both the Birthing and Newborn Centre at RVC and the RVAP Emergency. This will mean that we will be able to start to train and hire staff to support these new expansions in the new year.
We do have these as well, but fewer than we used to! We are better at managing them. Among our weaknesses are:
• Complacency – This is always a risk, but one that we are training ourselves away from with increasing Lean initiatives and successes of 2009 and 2008 to build on.
• Losing focus – We must relentlessly focus on improving the quality of care we deliver and we must continue to manage our operating costs diligently and carefully.
• Accountability for results is a mindset that we continue to develop. This includes greater transparency, staff empowerment and improved information for decision-making all supported by our Lean philosophy.
• Crisis management often dominates the time of our leadership team. Through Lean management we will shift our focus from fire-fighting to strategy and innovation.
Remember that every weakness is in fact, an opportunity for us to improve!
This is my favourite category.
• Our first opportunity is to continue building on our expertise in Lean management. This will be increasingly important as we continue to drive the quality agenda while managing through the inevitable effects of the recession. We will continue to develop our skills by integrating Lean training and education into our Management and Leadership competency development program called Advanced Leadership Foundations.
• Increased marketing of our regional centres of excellence in cardiac care and mental health. We will start to develop plans for the broader marketing of our services and strengthening our brand to one that represents the highest quality of care.
• Improving conservable days – meaning getting our patients home sooner. The reasons to reduce conservable days are simple and vital: timely discharges are good for patients as they recover better at home; it lowers their risk of infection; it makes beds available sooner to patients waiting in the emergency department; and it lowers costs to the hospital.
• MRI at RVAP. We are actively building our case to get ministry approval to have Magnetic Resonance Imaging services at RVAP. This is supported strongly by our hospital Board of Directors and is a priority item within our CE LHIN. Our RVHS Foundation is also ready to take on the challenge of fundraising for this vital equipment.
• Additional medical beds at RVAP. We are also actively working with the CE LHIN to add more medical beds at our RVAP campus to meet the demands of our growing community, improve access to critical care beds in Durham and to make the most of our new redevelopment space for the community.
• Continued practice of our ARC (Accountability, Respect and Caring) training. In short, let’s live our values every day: Responsive, respectful and caring to our patients, colleagues and community.
Threats are essentially the reverse of our opportunities, which I’ve just highlighted but there are some other significant threats that I need to talk about:
• Not achieving our Deficit Elimination Plan (DEP), which is entering its third and final year. We must achieve our annual financial targets, as we set out to do in March 2008, if we are going to meet our balanced budget responsibilities. We remain committed to our goals and will begin implementation of the third year of the plan in early January 2010. This will include further position reductions, but we will again minimize the number of involuntary exits through several redeployment strategies including the placement of staff into new positions created through the funding for the Birthing and Newborn Centre at RVC and the RVAP redevelopment. We must meet our DEP targets if we are to generate the cash we need to replace aging equipment and aging infrastructure, which you all deal with every day. We also have to be prepared to deal with the uncertainties in funding that may materialize next year. I will issue a blog on this early in the new year as well as hold Town Halls for broader discussion with staff, physicians and volunteers.
• Funding challenges. We’re certainly not alone in this boat. But we are better positioned, if we achieve our Deficit Elimination Plan, to respond to this threat. The Province, like all levels of government, has been severely constrained by the recession of 2008/09. Economic growth and catch up will take several years. It is possible that we will not receive the usual two per cent inflationary increase to our base funding next year, or potentially the year after. This will obviously mean that further cost containment, beyond the DEP, will be necessary if this scenario materializes. We are in fact planning for various funding scenarios (0%, 1% and 2 % increases) as instructed by the Joint OHA/LHIN H-SAA Steering Committee. However, it is important to understand that no decisions have yet been taken by government. Again I will let you know in the new year as this situation becomes clearer.
• As mentioned above, we have aging and previously neglected equipment and facilities, which will continue to require appropriate replacement and maintenance. We are factoring this in to our corporate plans. Clearly, part of the solution is the continued generation of operating surpluses to allow us to reinvest in our equipment and facilities. Without this reinvestment, keeping the lights on and continuing to provide high quality care will be difficult!
I thank you for your teamwork, your energy, spirit and collective wisdom during 2009.
Undoubtedly 2010 will be yet another year of challenge for our industry and RVHS. As a team we are stronger and better prepared to meet these challenges and the quality of care we are delivering is improving every day thanks to all of your efforts.
I wish you both health and happiness in 2010. All the best to you, your family and RVHS in the new year.
Monday, December 21, 2009
White Beans: White beans pack 20% of your daily value into a 1/2 cup serving. They are great added to soups and chilis, or tossed with vinaigrette and spinach for a white bean salad.
Broccoli: A 1/2 cup of frozen, fresh or steamed broccoli offers 15% of your daily folate value! Roast it with garlic as a side dish, toss fresh florettes into your salad or your favorite pasta dish.
Keep it Fresh!
Saturday, December 19, 2009
One famous study that supported this hypothesis was Ancel Keys's Seven Countries Study, conducted between the 1950s and 1970s. This study eventually served as the foundation on which much of the advice that we receive today from doctors is based, even though several other studies have been published since that provide little support for the lipid hypothesis.
The graph below (source: canibaisereis.com, with many thanks to O Primitivo) shows the results of one study, involving many more countries than Key's Seven Countries Study, that actually suggests a NEGATIVE linear correlation between total cholesterol and cardiovascular disease.
Now, most relationships in nature are nonlinear, with quite a few following a pattern that looks like a U-curve (plain or inverted); sometimes called a J-curve pattern. The graph below (source also: canibaisereis.com) shows the U-curve relationship between total cholesterol and mortality, with cardiovascular disease mortality indicated through a dotted red line at the bottom.
The total mortality curve is the one indicated through the full blue line at the top. In fact, it suggests that mortality increases sharply as TC decreases below 200.
Now, these graphs relate TC with disease and mortality, and say nothing about LDL cholesterol (LDL). In my own experience, and that of many people I know, a TC of about 200 will typically be associated with a slightly elevated LDL (e.g., 110 to 150), even if one has a high HDL cholesterol (i.e., greater than 60).
Yet, most people who have a LDL greater than 100 will be told by their doctors, usually with the best of the intentions, to take statins, so that they can "keep their LDL under control". (LDL levels are usually calculated, not measured directly, which itself creates a whole new set of problems.)
Alas, reducing LDL to 100 or less will typically reduce TC below 200. If we go by the graphs above, especially the one showing the U-curves, these folks' risk for cardiovascular disease and mortality will go up - exactly the opposite effect that they and their doctors expected. And that will cost them financially as well, as statin drugs are expensive, in part to pay for all those TV ads.
This year I got creative in the kitchen and baked my vegan peanut butter oatmeal cookies for everyone. Unfortunately, because of the snow today, 'Christmakuh' has been rescheduled! No worries though, I have the cookies safely stowed in the freezer until we meet to celebrate.
Here is my yummy, cruelty-free recipe. Enjoy and have a wonderful holiday!
Lauren's Peaceful Peanut Butter-Oatmeal Cookies
2 cups unbleached white whole wheat flour
2 cups rolled oats
2 teaspoons baking powder
1 teaspoon salt
3/4 canola oil (non-GMO of course!)
3/4 cup chunky all-natural peanut butter (my favorite is Smart Balance!)
1 cup granulated sugar
1/2 cup vanilla soy milk
2 teaspoons vanilla extract
1/2 cup grain sweetened chocolate chips
1/2 cup chopped walnuts
Preheat oven to 350°F. Lightly grease two cookie sheets.
Toss together the flour, oats, baking powder, nuts, chocolate chips, and salt in a large mixing bowl.
In a separate bowl mix together the oil, peanut butter, sugars, soy milk, and vanilla.
Add the dry ingredients to the wet, and mix. The dough will be very firm and moist.
Scoop a heaping tablespoon of dough and round with hand, then place onto cookie sheet. Gently flatten each cookie to a 1/2-inch thickness. Bake for 8 to 10 minutes.
Allow to cool at least 10 minutes for firm up before moving off the cookie sheet.
Keep it fresh!
Wednesday, December 16, 2009
Clementines are a sweet citrus fruit available throughout the wintertime, mid-November through March. One clementine is only about fifty calories. They are packed with fiber, vitamin C, folate, and potassium. They are also very rich in antioxidants such as beta-carotene as well as ascorbic acid, nutrients which when consumed on a daily basis reduces age-related vision loss.
History & Trivia
The history of the clementine is unclear in many ways. Some believe it was an Algerian monk that first discovered the natural hybrid fruit. (Clementines are a hybrid between a sweet orange and a Chinese mandarin.) Others believe that the clementine originated in China much earlier. Either way, in 1909, the fruit came to the USA, and is now enjoyed as a winter favorite by Americans everywhere. The majority of clementines are imported from Spain, Morocco and North Africa. Although its always better to eat locally grown produce, we can make an acceptation for these!
Selection & Storage Tips
Clementines should be bright orange and slightly glossy. Purchase those that are firm, yet give a slight indentation when you squeeze them. Make sure they have no blemishes, and especially no shriveled skin. They can be stored up to a week in a bowl at room temperature. They will last two weeks in the refrigerator. Clementines make a great snack anytime, and are also a nice addition to salads, both fruit salads and green, leafy salads. The juice of clementines can be added to salad dressings for a sweet, refreshing tang! However you prefer your clementines, enjoy them all through the winter while they are at their best!
Keep it Fresh!
Tuesday, December 15, 2009
It is mornings like these that I realize the simplicity of things, especially cooking. Using fresh, local ingredients makes it so easy and healthy. It is so satisfying to wake up and be able to indulge in such a breakfast. But it is also makes me feel a bit guilty. It makes me wonder how so many people can be hungry here when there is such an abundance of healthy whole foods.
I had the opportunity to find out the answer to that question over the last two weeks as I helped Gardens For Health International (GHI) conduct surveys of households all over the city, to whom they provide assistance. I got to see a lot of Kigali, and meet some amazing people in the process. An experience that certainly was a reminder of how much we take for granted.
GHI partners with 10 different co-ops throughout Kigali, all of which provide land for households with at least one member suffering from HIV. The land is used to grow crops in order to provide food security and nourishment to support their treatment. Throughout the course of the week I was paired up with a young Rwandan temp named Alfred, to conduct surveys in these households to help get a better idea of what foods they eat, what foods they grow, and if the gardens supplied by GHI are aiding in their adherence to treatment.
I knew that life here in Kigali was simple and that its people didn’t have much, but I don’t think you can ever really be prepared to witness the reality of life in an underdeveloped African nation. Nor do I think I could ever do it justice in writing, but I feel the need to try. However, in an effort to keep these blog posts short(er), I will describe my experience in a series of entries over the next week. An experience that has made me appreciate what I have, and realize how life here can be so difficult and so simple at the same time. So stay tuned!
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Monday, December 14, 2009
The fact is, the vast majority of high-quality observational studies have found no connection whatsoever between saturated fat consumption and heart attack risk. The scientific literature contains dozens of these studies, so let's narrow the field to prospective studies only, because they are considered the most reliable. In this study design, investigators find a group of initially healthy people, record information about them (in this case what they eat), and watch who gets sick over the years.
A Sampling of Unsupportive Studies
Here are references to ten high-impact prospective studies, spanning half a century, showing no association between saturated fat consumption and heart attack risk. Ignore the saturated-to-polyunsaturated ratios, Keys/Hegsted scores, etc. What we're concerned with is the straightforward question: do people who eat more saturated fat have more heart attacks? Many of these papers allow free access to the full text, so have a look for yourselves if you want:
A Longitudinal Study of Coronary Heart Disease. Circulation. 1963.
Diet and Heart: a Postscript. British Medical Journal. 1977. Saturated fat was unrelated to heart attack risk, but fiber was protective.
Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii. American Journal of Clinical Nutrition. 1978.
Relationship of Dietary Intake to Subsequent Coronary Heart Disease Incidence: the Puerto Rico Heart Health Program. American Journal of Clinical Nutrition. 1980.
Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study. New England Journal of Medicine. 1981.
Diet and 20-year Mortality in Two Rural Population Groups of Middle-Aged Men in Italy. American Journal of Clinical Nutrition. 1989. Men who died of CHD ate significantly less saturated fat than men who didn't.
Diet and Incident Ischaemic Heart Disease: the Caerphilly Study. British Journal of Nutrition. 1993. They measured animal fat intake rather than saturated fat in this study.
Dietary Fat and Risk of Coronary Heart Disease in Men: Cohort Follow-up Study in the United States. British Medical Journal. 1996. This is the massive Physicians Health Study. Don't let the abstract fool you! Scroll down to table 2 and see for yourself that the association between saturated fat intake and heart attack risk disappears after adjustment for several factors including family history of heart attack, smoking and fiber intake. That's because, as in most modern studies, people who eat steak are also more likely to smoke, avoid vegetables, eat fast food, etc.
Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. New England Journal of Medicine. 1997. From the massive Nurse's Health study. This one fooled me for a long time because the abstract is misleading. It claims that saturated fat was associated with heart attack risk. However, the association disappeared without a trace when they adjusted for monounsaturated and polyunsaturated fat intake. Have a look at table 3.
Dietary Fat Intake and Early Mortality Patterns-- Data from the Malmo Diet and Cancer Study. Journal of Internal Medicine. 2005.
I just listed 10 prospective studies published in top peer-reviewed journals that found no association between saturated fat and heart disease risk. This is less than half of the prospective studies that have come to the same conclusion, representing by far the majority of studies to date. If saturated fat is anywhere near as harmful as we're told, why are its effects essentially undetectable in the best studies we can muster?
Studies that Support the Diet-Heart Hypothesis
To be fair, there have been a few that have found an association between saturated fat consumption and heart attack risk. Here's a list of all four that I'm aware of, with comments:
Ten-year Incidence of Coronary Heart Disease in the Honolulu Heart Program: relationship to nutrient intake. American Journal of Epidemiology. 1984. "Men who developed coronary heart disease also had a higher mean intake of percentage of calories from protein, fat, saturated fatty acids, and polyunsaturated fatty acids than men who remained free of coronary heart disease." The difference in saturated fat intake between people who had heart attacks and those who didn't, although statistically significant, was minuscule.
Diet and 20-Year Mortality From Coronary Heart Disease: the Ireland-Boston Diet-Heart Study. New England Journal of Medicine. 1985. "Overall, these results tend to support the hypothesis that diet is related, albeit weakly, to the development of coronary heart disease."
Relationship Between Dietary Intake and Coronary Heart Disease Mortality: Lipid Research Clinics Prevalence Follow-up Study. Journal of Clinical Epidemiology. 1996. "...increasing percentages of energy intake as total fat (RR 1.04, 95% CI = 1.01 – 1.08), saturated fat (RR 1.11, CI = 1.04 – 1.18), and monounsaturated fat (RR 1.08, CI = 1.01 – 1.16) were significant risk factors for CHD mortality among 30 to 59 year olds... None of the dietary components were significantly associated with CHD mortality among those aged 60–79 years." Note that the associations were very small, also included monounsaturated fat (like in olive oil), and only applied to the age group with the lower risk of heart attack.
The Combination of High Fruit and Vegetable and Low Saturated Fat Intakes is More Protective Against Mortality in Aging Men than is Either Alone. Journal of Nutrition. 2005. Higher saturated fat intake was associated with a higher risk of heart attack; fiber was strongly protective.
The Review Papers
Over 25 high-quality studies conducted, and only 4 support the diet-heart hypothesis. If this substance is truly so fearsome, why don't people who eat more of it have more heart attacks? In case you're concerned that I'm cherry-picking studies that conform to my beliefs, here are links to review papers on the same data that have reached the same conclusion:
The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease. Journal of Clinical Epidemiology. 1998. Dr. Uffe Ravnskov challenges the diet-heart hypothesis simply by collecting all the relevant studies and summarizing their findings.
A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine. 2009. "Insufficient evidence (less than or equal to 2 criteria) of association is present for intake of supplementary vitamin E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total fat; alpha-linolenic acid; meat; eggs; and milk" They analyzed prospective studies representing over 160,000 patients from 11 studies meeting their rigorous inclusion criteria, and found no association between saturated fat consumption and heart attack risk.
Where's the Disconnect?
The first part of the diet-heart hypothesis states that dietary saturated fat raises the cholesterol/LDL concentration of the blood. The second part states that increased blood cholesterol/LDL increases the risk of having a heart attack. What part of this is incorrect?
There's definitely an association between blood cholesterol/LDL level and heart attack risk in certain populations, including Americans. MRFIT, among other studies, showed this definitively, although the lowest risk of all-cause mortality was at an average level of cholesterol.
So we're left with the first premise: that saturated fat increases blood cholesterol/LDL. This may be a short-term effect, and it isn't necessarily true in animal models of heart disease if you exclude those that use large doses of dietary cholesterol. In the 1950s, Dr. Ancel Keys created a formula designed to predict changes in blood cholesterol based on the consumption of dietary saturated and polyunsaturated fats. However, it has shown limited predictive value in long-term diet modification trials such as MRFIT and the Women's Health Initiative.
Friday, December 11, 2009
This week's Friday Friends Shout Out goes to Real Mama, Inc. based in Middletown, NJ. Real Mama, Inc. is an environmental and kids health non-profit organization comprised of a group of truly amazing women, including Cornelia Mazzan, Kirstin McPolin, Kari Martin and Camille Lofaro Sowinski who have made it their mission to inform and educate mothers and families about how to integrate environmental stewardship into everyday life. Their ultimate goes is to increase the health of families as well as the awareness and conservation of the natural environment through the most important resources we have, our children!
Real Mama publishes a quarterly web-based eNewsletter that provides information specifically tailored to meet the needs of busy mothers and caregivers. Their articles present a summarized, balanced view of issues that are easily digestible so you can actually act on the information provided.
On December 17, Real Mama is hosting a Wine Tasting & Food Pairing at Whole Foods Market in Middletown, NJ; Affordable Wines and Green Minds for Holiday Celebrating. The tasting will include wine and food pairings throughout the store featuring sustainable, affordable wines and tastey bites for the upcoming holiday season. You can register for the tasting here.
3 Healthy Chicks want to thank Real Mamas for making our community and kids a happier and healthier place. Keep doing what you're doing. We think you're fabulous!!!
Keep it Fresh
Wednesday, December 9, 2009
Tuesday, December 8, 2009
My doctor gave me the standard advice in these cases: exercise, lose weight, and, most importantly, reduce your intake of saturated fat. I was also told that I would probably have to take statins, as my high LDL likely had something to do with my genetic makeup. Again, this is quite standard, and we see it all over the place, particularly in commercials for statins.
I told my doctor that I would do some research on the topic, which I am going to save for other posts. Let me get to the point, by telling you what my lipid profile is today - LDL: 123, HDL: 66, triglycerides: 46. Again, the LDL value is calculated. I am weighing about 152 lbs now, with about 13 percent of body fat.
The HDL and triglycerides numbers above are shown in bold font because my research convinced me that these two numbers are the ones most people should really worry about when trying to address what is known as dyslipidemia. Here I am assuming that only standard lipid profiles are available; there are better alternatives, such as particle type analyses, which are not yet standard.
Many people who suffer from cardiovascular disease have low LDL cholesterol, but very few of those have high HDL cholesterol, which is one of the best predictors of cardiovascular disease among lipids. More specifically, if you have an HDL higher than 60, you have a very small chance of developing cardiovascular disease. (It can happen, but it is very unlikely, with a percentage chance in the single digits.)
Interestingly, low HDL cholesterol is also associated with the metabolic syndrome. This syndrome is characterized by the following:
- High fasting serum glucose (hyperglycemia), which is one of many signs of insulin resistance, a precursor to diabetes type 2;
- High blood pressure;
- Abdominal obesity (also known as pot or beer belly);
- Low HDL cholesterol; and
- Elevated triglycerides.
Now, you may ask, how did you increase your HDL? Well, I tried a number of things - diet and lifestyle changes - and had a blood test every 3 months. After a while I was able to put all of the measures in a spreadsheet table, and correlate them using a statistical software that I developed, to give me an idea of what was going on.
Weight was a big factor on LDL, and I was able to bring my weight down to 150 lbs and my LDL to below 100 at some point. For me, and many other people, body weight and LDL cholesterol are strongly and positively correlated (the higher the weight, the higher the LDL cholesterol - actually body fat seems to be the real culprit). Moreover, my LDL seemed to decrease more markedly when my weight was on the way down, and not as much when it was stable, even if low.
But the HDL would only increase if I increased my saturated fat intake. The problem is that every time I increased my saturated fat intake my LDL would go up; it reached 162 at one point, when my HDL went up to a modest but encouraging 47. That was my highest HDL until I eliminated refined carbs and sugars (e.g., bread, pasta, cereals, doughnuts, bagels, regular sodas) from my diet.
When I brought my intake of refined carbs and sugars down to zero, my intake of protein and saturated fat went up. Either that would happen, or I would starve, because you have to eat something. (I figured that I would not die by doing a low carb/high fat-protein experiment for 3 months to see what happened.) Also, I dramatically increased my dietary cholesterol - two to four eggs per day, organ meats, and seafood.
That is when my HDL shot up, to 66, and my LDL went down. Yes, my LDL levels seem to be negatively correlated with dietary saturated fat and cholesterol amounts, as long as I do not consume refined carbs and sugars. Moreover, it is very likely that my LDL particle size increased, and large LDL particles DO NOT cause atherosclerosis because they cannot penetrate the artery walls.
So, the bottom line is that, at least for me, an INCREASE in saturated fat and a DECREASE in refined carbs and sugars, happening together, seem to have taken me out of my previous path toward the metabolic syndrome.
Moreover, I feel a lot more energetic than before, my immune system seems to have gotten better at fighting disease, and even my pollen allergies are not as bad as they were before. Admittedly, these benefits may be strongly associated with the weight loss and the related reduction in body fat percentage.
I hope this post is helpful to others. The standard advice that people with high LDL cholesterol receive, which usually focuses on reducing saturated fat intake, has a big problem. When you reduce your intake of a type of food, you usually increase your intake of other types of food. Most people who try to reduce their saturated fat intake invariably increase their carb intake, usually with the wrong types of carb-rich foods (the man-made ones), simply because they go hungry.
Monday, December 7, 2009
Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). Here's a graph of the percent body fat over time of the two groups:
The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell.
Butyrate lowered their blood cholesterol by approximately 25 percent, and their triglycerides by nearly 50 percent. It lowered their fasting insulin by nearly 50 percent, and increased their insulin sensitivity by nearly 300 percent*. The investigators concluded:
Butyrate and its derivatives may have potential application in the prevention and treatment of metabolic syndrome in humans.There's one caveat, however: the butyrate group at less food. Something about the butyrate treatment caused their food intake to decline after 3 weeks, dropping roughly 20% by 10 weeks. The investigators cleverly tried to hide this by normalizing food intake to body weight, making it look like the food intake of the comparison group was dropping as well (when actually it was staying the same as this group was gaining weight).
I found this study thought-provoking, so I looked into butyrate further.
Butyrate Suppresses Inflammation in the Gut and Other Tissues
In most animals, the highest concentration of butyrate is found in the gut. That's because it's produced by intestinal bacteria from carbohydrate that the host cannot digest, such as cellulose and pectin. Indigestible carbohydrate is the main form of dietary fiber.
It turns out, butyrate has been around in the mammalian gut for so long that the lining of our large intestine has evolved to use it as its primary source of energy. It does more than just feed the bowel, however. It also has potent anti-inflammatory and anti-cancer effects. So much so, that investigators are using oral butyrate supplements and butyrate enemas to treat inflammatory bowel diseases such as Crohn's and ulcerative colitis. Investigators are also suggesting that inflammatory bowel disorders may be caused or exacerbated by a deficiency of butyrate in the first place.
Butyrate, and other short-chain fatty acids produced by gut bacteria**, has a remarkable effect on intestinal permeability. In tissue culture and live rats, short-chain fatty acids cause a large and rapid decrease in intestinal permeability. Butyrate, or dietary fiber, prevents the loss of intestinal premeability in rat models of ulcerative colitis. This shows that short-chain fatty acids, including butyrate, play an important role in the maintenance of gut barrier integrity. Impaired gut barrier integrity is associated with many diseases, including fatty liver, heart failure and autoimmune diseases (thanks to Pedro Bastos for this information-- I'll be covering the topic in more detail later).
Butyrate's role doesn't end in the gut. It's absorbed into the circulation, and may exert effects on the rest of the body as well. In human blood immune cells, butyrate is potently anti-inflammatory***.
Butyrate Increases Resistance to Metabolic and Physical Stress
Certain types of fiber reduce atherosclerosis in animal models, and this effect may be due to butyrate production produced when the fiber is fermented. Fiber intake was associated with lower blood markers of inflammation in the Women's Health Initiative study, and has been repeatedly associated with lower heart attack risk and reduced progression of atherosclerosis in humans. Butyrate also sharply reduces the harmful effects of type 1 diabetes in rats, as does dietary fiber to a lesser extent.
Butyrate increases the function and survival of mice with certain neurodegenerative diseases. Polyglutamine diseases, which are the most common class of genetic neurodegenerative diseases, are delayed in mice treated with butyrate (1, 2, 3). Many of you have probably heard of Huntington's disease, which is the most common of the class. I did my thesis on a polyglutamine disease called SCA7, and this is the first suggestion I've seen that diet may be able to modify its course.
Yet another interesting finding in the first paper I discussed: mice treated with butyrate were more cold-resistant than the comparison group. When they were both placed in a cold room, body temperature dropped quite a bit in the comparison group, while it remained relatively stable in the butyrate group, despite the fact that the butyrate group was leaner****. This was due to increased heat production in the butyrate group.
Due to the potent effect butyrate has on a number of bodily processes, I believe it may be a fundamental controller of metabolism, stress resistance and the immune system in mammals, similar to omega-6:3 balance.
An Ancient Line of Communication Between Symbiotic Organisms
Why does butyrate have so much control over inflammation? Let's think about where it comes from. Bacteria in the gut produce it. It's a source of energy, so our bodies take it up readily. It's one of the main molecules that passes from the symbiotic (helpful) bacteria in the gut to the rest of the body. It's only logical that the body would receive butyrate as a signal that there's a thriving colony of symbiotic bacteria in the gut, and induce a tolerance to them. The body may alter its immune response (inflammation) in order to permit a mutually beneficial relationship between itself and its symbionts.
A Change of Heart
Butyrate has caused me to re-think my position on fiber-- which was formerly that it's irrelevant at best. I felt that fiber came along with nutrient-dense whole plant foods, but was not beneficial per se. I believed that the associations between fiber intake and a lower risk of a number of diseases were probably due to the fact that wealthier, more educated, healthier people tend to buy more whole grains, fruit and vegetables. In other words, I believed that fiber intake was associated with better health, but did not contribute to it. I now feel, based on further reading about fiber and short-chain fatty acids like butyrate, that the associations represent a true cause-and-effect relationship.
I also didn't fully appreciate the caloric contribution of fiber to the human diet. In industrialized countries, fiber may contribute 5 to 10 percent of total calorie intake, due to its conversion to short-chain fatty acids like butyrate in the large intestine (free full text). This figure is probably at least twice as high in cultures consuming high-fiber diets. It's interesting to think that "high-carbohydrate" cultures may be getting easily 15 percent of their calories from short-chain fats. Since that isn't recorded in dietary surveys, they may appear more dependent on carbohydrate than they actually are. The Kitavans may be getting more than 30 percent of their total calories from fat, despite the fact that their food is only 21 percent fat when it passes their lips. Their calorie intake may be underestimated as well.
Sources of Butyrate
There are two main ways to get butyrate and other short-chain fatty acids. The first is to eat fiber and let your intestinal bacteria do the rest. Whole plant foods such as sweet potatoes, properly prepared whole grains, beans, vegetables, fruit and nuts are good sources of fiber. Refined foods such as white flour, white rice and sugar are very low in fiber. Clinical trials have shown that increasing dietary fiber increases butyrate production, and decreasing fiber decreases it (free full text).
Butyrate also occurs in significant amounts in food. What foods contain butyrate? Hmm, I wonder where the name BUTYR-ate came from? Butter perhaps? Butter is 3-4 percent butyrate, the richest known source. But everyone knows butter is bad for you, right?
After thinking about it, I've decided that butyrate must have been a principal component of Dr. Weston Price's legendary butter oil. Price used this oil in conjunction with high-vitamin cod liver oil to heal tooth decay and a number of other ailments in his patients. The method he used to produce it would have concentrated fats with a low melting temperature, including butyrate, in addition to vitamin K2*****. Thus, the combination of high-vitamin cod liver oil and butter oil would have provided a potent cocktail of fat-soluble vitamins (A, D3, K2), omega-3 fatty acids and butyrate. It's no wonder it was so effective in his patients.
* According to insulin tolerance test.
** Acetate (acetic acid, the main acid in vinegar), propionate and butyrate are the primary three fatty acids produced by intestinal fermentation.
*** The lowest concentration used in this study, 30 micromolar, is probably higher than the concentration in peripheral serum under normal circumstances. Human serum butyrate is in the range of 4 micromolar in British adults, and 29 micromolar in the hepatic portal vein which brings fats from the digestive tract to the liver (ref). This would likely be at least two-fold higher in populations eating high-fiber diets.
**** Due to higher mitochondrial density in brown fat and more mitochondrial uncoupling.
***** Slow crystallization, which selectively concentrates triglycerides with a low melting point.