Ease off the fats during pregnancy

Obesity remains one of the primary headlines every day. But what you probably don’t know is the fastest growing segment of the obesity epidemic is children less than 4 years old. Approximately 20 percent are obese (1). Even more disturbing is the growth of obesity in children under the age of six months (2). You can’t blame school lunch programs for this youngest group, since they are too young to go to school, and you can’t blame lack of exercise since they can’t walk yet.

Frankly, no child wants to be obese. In fact, their quality of life is similar to that of a child undergoing chemotherapy (3). Yet we are constantly reminded that they are obese because they lack personal responsibility, and they only have to “eat less and exercise more”. The fact that such interventions don’t seem to work is simply a minor detail (4-6).

As I mentioned in an earlier blog, the culprit may be fetal programming in the womb that is causing epigenetic changes in the fetus before birth. This has already been demonstrated in pregnant rats that were fed a high-fat diet from the first day of pregnancy (7). These rats were genetically bred to be obesity resistant so that extra fat in their diet didn’t increase the body weight of the mothers during pregnancy. However, the offspring of those mothers fed the high-fat diet had blood sugar levels that were nearly twice as high as compared to offspring coming from the pregnant rats being fed a normal-fat diet. This is an indication that they were born with insulin resistance.

When researchers looked for epigenetic markers that might distinguish the two groups of offspring, sure enough they found chemical markers in the genes that regulate glucose metabolism. Since these epigenetic markers on the genes are not easily removed, the offspring with them would face a lifetime of dietary challenge to counteract their new genetic pre-disposition to obesity and diabetes.

So let’s come back to the growing childhood obesity problem in the very young. It may be due to fetal programming caused by high levels of both saturated and omega-6 fatty acids in the prenatal diet. Both types of fatty acids will cause increased cellular inflammation that can affect gene expression. If that occurs in the fetus, then that may be enough to genetically alter their future for a lifetime, including a far greater risk of obesity and diabetes.

References

  1. Anderson SE and Whitaker RC. “Prevalence of Obesity Among US Preschool Children in Different Racial and Ethnic Groups.” Arch Pediatric Adolescent Med 163: 344-348 (2009)
  2. Kim J, Peterson KE, Scanlon KS, Fitzmaurice GM, Must A, Oaken E, Rifas-Shiman SL, Rich-Edwards JW, and Gillman MW. “Trends in overweight from 1980 through 2001 among preschool-aged children enrolled in a health maintenance organization.” Obesity 14: 1107-1112 (2006)
  3. Schwimmer JB, Burwinkle TM, and Varni JW. “Health-related quality of life of severely obese children and adolescents.” JAMA 289: 1813-1819 (2003)
  4. McGovern L, Johnson JN, Paulo R, Hettinger A, Singhal V, Kamath C, Erwin PJ, and Montori VM. “Clinical review: treatment of pediatric obesity: a systematic review and meta-analysis of randomized trials.” J Clin Endocrinol Metab 93: 4600-4605 (2008)
  5. Kamath CC, Vickers KS, Ehrlich A, McGovern L, Johnson J, Singhal V, Paulo R, Hettinger A, Erwin PJ, and Montori VM. “Clinical review: behavioral interventions to prevent childhood obesity: a systematic review and meta-analyses of randomized trials.” J Clin Endocrinol Metab 93: 4606-4615 (2008)
  6. Shaw K, Gennat H, O’Rourke P, and Del Mar C. “Exercise for overweight or obesity.” Cochrane Database Syst Rev 2006: CD003817 (2006)
  7. Strakovsky RS, Zhang X, Zhou D, and Pan YX. “Gestational high-fat diet programs hepatic phosphoenolpyruvate carboxykinase gene expression and histone modification in neonatal offspring rats.” J Physiol 589: 2707-2717 (2011)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

What are we really entitled to?

For the past year the future of the American economy has centered on the word “entitlement,” especially in terms of health care. But no one is quite certain about what the word means. Social Security is not really an entitlement because it is a forced savings program that promises you the money you put into an old-age fund will be given back to you when you need it, some time in your 60s. The fact that the government has been using that account as a piggy bank to fund itself without raising taxes and leaving behind government I.O.U.s in place of the funds is another matter. But you are definitely entitled to at least get back the money you put into it.

Medicare is a completely different matter. In this case, you put very little money into a fund (which is also heavily borrowed from by the government), and you expect to get a lot more back. In my view, you are entitled to get back the money you paid into Medicare, and anything more should be considered a gift from a rich uncle (Sam), who is no longer very rich.

In an attempt to resolve this problem, Congressman Paul Ryan came up with a plan that went nowhere but had at least some intellectual merit: You pay into the medical fund for old age, and you get back what you paid in (and a little more) at age 67. The most notable feature of this plan was getting an annual voucher for about $6,000 based on 2012 dollars to be applied for private health insurance premiums after age 67.

At the current Medicare tax rate, the only way to pay in more than $6,000 into proposed trust fund on an annual basis is if you make more than $200,000 per year. Since there aren’t too many Americans making that type of salary, it’s your rich uncle who must make up the difference. Even if you were making $200,000 per year for 40 years and only planned to live another 15 years after retirement, it is still a pretty good deal, as it is forced savings for health-care insurance in the future. Any overpayment on your part will only help those who are not lucky enough to make $200,000 a year for 40 years. Unfortunately, this proposal was politically dead on arrival

The real problem with any health-care entitlement program was pointed out in a well-reasoned article in the May 19th issue of The New Republic — you can’t cure chronic disease, you can only manage it (1). In addition, new research analyses of the current state of Americans in old age indicates that we aren’t doing a very good job of managing chronic diseases (2). Although Americans are living longer, the length of life with chronic disease and loss of functional mobility (i.e. independent living) have rapidly increased since 1998. We are living longer because the elderly are essentially on life support generated by increasingly more expensive drugs that only marginally extend the lives of the very sick. We are not going to cure heart disease, cancer, stroke, and definitely not Alzheimer’s. The best we can do is to help manage their outcomes. Unfortunately, these are also diseases of the elderly, and the cost of increasing each year of life after 65 has risen from about $50,000 in the 1970s to nearly $150,000 in the 1990s. This could possibly be justified if the rich uncle were still rich.

The solution according to the authors of the New Republic article is redirecting the money that we can spend to maximize expenditures on public health care (prevention and elongation of independent living) as opposed to “curing” elderly with chronic disease that usually results in the decreased quality of life (1). The primary beneficiaries of this shift in medical thinking should be children followed by working adults, with the lowest health-care priority going to those over age 80. It sounds harsh, but that is exactly how socialized medicine works in Europe.

So what do you do to protect yourself in the future, especially if you are nearing 65? My suggestion is to start aggressively reducing cellular inflammation by following an anti-inflammatory diet and lifestyle. That’s the only thing you are really entitled to and that will also be the only thing your “rich” uncle can realistically pay for in the future.

References

  1. Callahan D and Nuland S. “The quagmire: how American medicine is destroying itself.” The New Republic. May 19, 2011
  2. Crimmins EM and Beltran-Sanchez H. “Mortality and morbidity trends: is there compression of morbidity?” J Gerontol B Physchol Soc Sci 66: 75-86 (2011)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Getting closer to the Zone all the time

Last week the USDA announced its newest version of how Americans should eat. For the first time in more than 20 years, the USDA apparently stopped acting as the marketing arm of agribusiness by using a food pyramid (presented in 1992) and worse yet some abstract concept of an “eat-more, exercise-more” idea (presented in 2005). Now the USDA has turned to a plate format, which I have used for years. For comparison, you can see that the Zone diet recommendations are still a lot easier to understand than even the new and improved USDA recommendations as shown below:

The USDA proposes that half your plate (I’ll assume at every meal that you want to control the glycemic load of the meal) should be composed of vegetables and fruits. This is much closer to my Zone recommendation of filling 2/3 of the plate at each meal with vegetables and fruits. Both plates give a volume size to protein (and I’ll assume it is a low-fat protein source). The Zone plate appears to have a higher amount of low-fat protein consisting of 1/3 the plate instead of a quarter as found in the USDA plate. Of course if you add in the strange circle outside the plate that represents milk or cheese (both protein sources) back onto the plate, then you would probably get to about 1/3 the plate volume as low-fat protein.

Finally, what about whole grains on the USDA plate? From a glycemic-load viewpoint, whole grains have nearly the same impact on insulin response as refined grains, so you really don’t gain anything hormonally from having them in your diet. However, if you are at your ideal percentage of body fat, have no chronic disease, perform at peak levels, and are always happy and even-keeled emotionally, only then should you think about adding some whole grains to your diet. (Keep in mind that real whole grains are usually only found in storage bins or in the frozen product section of the supermarket, not in the processed food aisles.) But if you begin to gain weight, develop indications of a chronic disease, or don’t perform physically, mentally, and emotionally on a consistent basis, then take the whole grains out of your diet and go back to my classic Zone plate.

The one thing not mentioned in the USDA guidelines is the role of fat. On the Zone plate, I always say add a dash (that’s a small amount), but that dash of fat should be very low in omega-6 and saturated fats as both can accelerate cellular inflammation. I guess the USDA hasn’t had time to grapple with that more complex dietary concept. Perhaps they will another five years from now. But you don’t have to wait for their next guideline revision. Just follow the dietary guidelines on the Zone plate the best you can at every meal and snack. If you do, then you have done everything possible to maintain your wellness (as measured by your ability to manage cellular inflammation) for as long as possible. I guarantee you that will be the only real health-care reform program that you can count on in the future.

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

Another new wrinkle in the cholesterol story

One of the great marketing successes of the pharmaceutical industry has been the linkage between LDL cholesterol levels and heart disease. In essence, the message, “if your LDL cholesterol is high, you are going to die,” is powerful. Unfortunately, the data state otherwise.

It was known in the mid 1990s that oxidized LDL was the primary suspect in the development of atherosclerotic lesions; not natural, non-oxidized LDL. But it was also at this time that the first statin studies began to appear, and that gave the pharmaceutical industry a patented drug to “prevent” heart disease (2). It was such a good story to tell and an even better one to sell. Unfortunately, as I pointed out in an earlier blog, it has never held up well against unbiased scrutiny, especially in patients with high cholesterol levels but without any heart disease.

Part of the reason lies in the data. Shown below is the correlation of LDL cholesterol to heart disease

You can see from this data that there is a higher percentage of cardiovascular disease patients with high LDL cholesterol levels compared with very low levels, but not that much. This explains why about half the people who die from heart disease have normal LDL cholesterol levels (less than 130 mg/dl). It also means that high LDL cholesterol is not a very good predictor of heart disease.

On the other hand, a very different picture emerges if you look at the levels of oxidized LDL levels as shown below.

Even without a background in statistics you can see a very striking relationship in the prediction of heart disease with increasing levels of oxidized LDL levels.

So why don’t physicians use oxidized LDL levels as an indicator of heart disease risk? First, the test is much more difficult to do than a simple cholesterol test. Second, it ruins a great story that is easy to communicate to the patient. Third, the best way of reducing oxidized LDL levels is natural anti-oxidants, such as polyphenols, that have no patent protection (3,4). Reducing LDL cholesterol is simple. Just take a statin drug for the rest of your life. Reducing oxidized LDL cholesterol requires having plenty of antioxidants in your diet with polyphenols the most powerful.

Now there is another new entry into the LDL story. This is “super-sticky” LDL. In an online pre-publication, it was demonstrated that this new type of LDL particle may be even worse than oxidized cholesterol in promoting the development of heart disease (5). This “super-sticky” LDL comes from the formation of advanced glycosylation end products (AGEs). I described this formation of protein-carbohydrate linkages as an integral part of the aging process in my book, “The Anti-Aging Zone,” published more than a decade ago (6).

The best way to reduce the production of “super-sticky” LDL is to reduce blood sugar levels. This helps explain why individuals with diabetes are two to three times more likely to develop heart disease. The best way to reduce elevated blood sugar is the Zone diet. That’s why the latest dietary recommendations for the treatment of diabetes by the Joslin Diabetes Research Center at Harvard Medical School are essentially identical to the Zone diet.

Heart disease remains the number-one cause of death in America. Unfortunately, it is more complex than “taking a statin a day to keep death away”.

References

  1. Maor I and Aviram M. “Oxidized low-density lipoprotein leads to macrophage accumulation of unesterified cholesterol as a result of lysosomal trapping of the lipoprotein hydrolyzed cholesterol ester.” J Lipid Res 35: 803-819 (1994)
  2. Simvastatin Study Group. “Randomized trial of cholesterol lowering in 4,444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S).” Lancet 344: 1383-1389 (1994)
  3. Shafiee M, Carbonneau MA, Urban N, Descomps B, and Leger CL. “Grape and grape seed extract capacities at protecting LDL against oxidation generated by Cu2+, AAPH or SIN-1 and at decreasing superoxide THP-1 cell production.” Free Radic Res 37: 573-584 (2003) (ISSN: 1071-5762)
  4. Chen CY, Yi L, Jin X, Mi MT, Zhang T, Ling WH, and Yu B. “Delphinidin attenuates stress injury induced by oxidized low-density lipoprotein in human umbilical vein endothelial cells.” Chem Biol Interact 183: 105-112 (2010)
  5. Rabbani N, Godfrey L, Xue M, Shaheen F, Geoffrion M, Milne R, and Thornalley PJ. “Glycation of LDL by methylglyoxal increases arterial atherogenicity.” Diabetes 60 doi:10.2337/db09-1455 (2011)
  6. Sears B. “The Anti-Aging Zone.” Regan Press. New York, NY (1999)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.