Posts

Aging and The Brain

coconut oil, fats oils, essential fatty acids

Our brains are 60% fat. In light of what we know of brain function and the essential fatty acids that are responsible, the term “fat-head” could now be a complement. Since our brains are in charge and require the right fats to run our thinking machinery, our first priority is to make sure we add the right ones into our diet, the omega 6s and omega 3s. They are essential and get the job done. First – let’s review some of the basics.

Fats and oils can be divided into two densities and two levels. The densities are not unlike the SAE oils, the Society of Automotive Engineers who organize the oils for our autos. But it is better to skip the details at the moment and divide them in two categories “thick” and “thin”. Fats are the thick ones and oils are thin, actually runny. It’s quite good to divide them in this simplistic way. The confusion about what we eventually eat is all over the lot and besides, our cells and membranes organize fats and oils as partners with each having a precise role. The membrane does not work without both, thick and thin, sluggish and active. We can begin with the ones we use in our kitchens because they wind up in our metabolism whether we like it or not.

You can think of the thick ones as butter or lard. We tend to look down on lard as being out of date. We regard it as a thing of the past. Our grandparents and great grandparents certainly didn’t think so. As cooking oil, lard has been with us for some time. It’s been a staple for centuries, probably hundreds of centuries, and we’ve survived and even flourished. It’s part of our evolutionary history. Those thick heavy oils were skimmed off the top of stews and saved, collected from roasts of pork, lamb, goose or turkey. It was regarded as valuable stuff. Before the light bulb, making candles was a basic part of life so the rendering of fat in the kitchen was universal. The plain fact is that lard is OK for cooking. However, just reminiscing, not pushing lard today.

Butter and olive oil are both excellent cooking oils, however, coconut is also marvelous for cooking. It’s not exactly a thick fat, for as you know, it quickly gets thin as the temperature rises. Castillo et al 1999, reports that “Supplementation of coconut oil produced a significant hypercholesterolemia after 7 days of treatment. However, supplementation of menhaden oil induced a significant decrease in total cholesterol after only 2 weeks of treatment”. The raising of cholesterol may sound sacrilegious; however, notwithstanding the loud din of media anti-cholesterol noise, there are those who have difficulty in doing just that – raising cholesterol. Cholesterol is an important fat for our cell membranes; it metabolizes up to our gonadal hormones — think sex. No necessity in elaborating on that subject. It’s also a precursor for our adrenal hormones, which produce our life saving impulses for fight or flight, and bile acids which shepherd the fats and oils around in the blood stream. Without further ado — cholesterol is necessary.

Castillo creates an interesting picture of coconut oil, or butter, as you prefer, and the essential oils that are part of our diet. By itself, coconut can raise cholesterol, but by introducing menhaden oil, it just as quickly reverses and lowers it. This feature of menhaden oil, basically an omega 3 essential fatty acid (EFAs), to lower cholesterol, is also duplicated with the omega 6 EFAs, and there is abundant research that corroborates it. We can regard all of the omega 6s and 3s as “thin oils” and cholesterol, when grouped together as a very “thick fat”.

The lesson here is more than casual. We need the thick ones and we desperately need the thin ones. The thin ones keep the thick ones from collecting to the degree where we tend to get into trouble that comes with aging, such as atherosclerosis, heart disease. In just these two words, thick and thin, we have covered half of all Fatty Acid biochemistry in human metabolism. But it may be just too simple to be looked at with the respect that it deserves. You may spend a third of your life getting a medical degree and half again practicing medicine, but if you do not see this simple relationship you will also retire as a failure from your chosen field of medicine.

Coconut used to be the preferred oil for making popcorn, but ADM and the other large oil producers chased it out of the movies over 30 years ago. It’s a shame we lost it. It was much healthier eating coconut oil than what is currently in use today. Most of the oils used for popcorn and fries are PUFAs, they are thin and should not be heated. They quickly degenerate and become partially hydrogenated and/or oxidize and become rancid.

Coconut oil is one of the most stable oils you can buy. It does not turn rancid easily. It does not attack your arteries. In fact, coconut oil was one of the foods Dr. Weston Price studied when he traveled the world searching for healthier people and their lifestyles. In his journeys he discovered that the coconut was considered a medicine food by the local populations. He found that those civilizations that consumed coconut regularly had no knowledge of cancer, heart disease, arthritis, or diabetes.

There are few other choices for cooking unless you think of the new GMO oils like high oleic soybean, sunflower or safflower oils, Canola also fits into that group because it was one of the first GMO oils to be converted. Canola contains erucic acid, a very long chain saturated fat. It is unhealthy for our membranes, it’s too long and slows the fluidity of the membrane. Think of erucic as a gawking fat blocking our healthy fats from doing what they want to do, running quickly in our membranes managing our cells. Please avoid canola. We simply do not like GMOs for anything we eat.

The thin oils, the PUFAs, come from seeds, nuts, and grains like olive, sunflower, corn, walnut, etc. They harbor the essential fatty acids which play a vital role when the time comes for them to reproduce new versions of themselves. Oils like olive are mostly Mono-Unsaturated Fatty Acids (MUFAs), and are OK, but do not stack up with the likes of the omega 6 and 3 PUFAs, the very healthy FAs. These Poly-Unsaturated Fatty Acids, with more than one double bond, are the stars in our choices of foods. They are predominantly made up of the essential oils, the omega 6s and the omega 3s and are exclusively made by plant seeds. They are important for life and especially the brain. When we use the term essential, we mean that the body cannot function without them. They are essential for life, our life. They hold the secret to Brain health, which we will delve into on Aging and the Brain: Part 2.

To learn more about one of the most important EFA discoveries of the last century, the ratio of 6s and 3s, which is 4: 1, 80% omega 6 (linoleic) to 20% omega 3 (linolenic), go tohttp://www.bodybio.com/BodyBio/docs/BodyBioBulletin-4to1Oil.pdf.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Soda and Obesity

type 2 diabetes, obesityWhile a major study relating soda and obesity was done in California, the hypothesis, observations and outcomes are applicable to all the states of the Union.  More than half the adolescents in that state and almost a fourth of the adults treat themselves to at least one sweetened beverage every day.  One of the concerns expressed by UCLA researchers is that the serving size has grown from an average of 6.5 ounces and eighty-eight calories in the 1950’s to 20 ounces and two hundred sixty-six calories by the 2000’s.  In fast food restaurants in 2003, the average serving was 23 ounces (almost 300 calories).  These added caloric sweeteners, including high fructose corn syrup, are not only markers of a poor diet, but also are associated with overweight and obesity in all age groups.

CITATIONS FROM REPORT / ARTICLE
The UCLA Health Policy Research Brief from September, 2009, reports from its data that, “Adults who drink soda occasionally (not every day) are 15% more likely to be overweight or obese, and adults who drink one or more sodas per day are 27% more likely to be overweight or obese than adults who do not drink soda, even when adjusting for poverty status and race/ethnicity.”  Even though the prevalence of overweight in children is lower than in adults, the rates among children have increased more.  In fact, overweight has tripled in teenagers and quadrupled in those from six to eleven years old in the last three decades.  In California the cost of obesity approaches twenty-one billion dollars a year, burdening families, employers and the health care industry.  The study comments that, “California spends more public and private money on the health consequences of obesity than any other state.”  To compound the matter, the article admits that “…drinking soda is also associated with increased risk for type 2 diabetes.”

COMMENTARY
One third of American adults are obese. Their health care costs $1500 more a year than it does for an average-weight person.  The Center for Disease Control announced in July, 2011, that obesity in the entire United States costs $147 billion a year in direct medical costs.  Dr. Thomas R. Frieden, director of the CDC, said the problem is “getting worse rapidly.  The average American is now 23 pounds overweight.”  For Medicare, the cost of obesity is 72% greater just for prescription drugs.  The CDC says that one in three children born in 2000 will develop diabetes.  How did we get there?  Diet.  Does the rest of the world share the problem?  Yes.  Where does the blame go?  White flour, white sugar, high fructose corn syrup, soft drinks and fast food.

Whether it gets marketed as corn sugar or as high fructose corn syrup, which is what it is, this commodity is not equal to other sweeteners when it comes to weight gain.  HFCS costs less than table sugar because, being liquid, it’s easier to transport and blend.  It’s sweeter than sucrose (table sugar), so less is needed, and it’s cheaper because of a combination of corn subsidies and sugar tariffs and quotas.  Cheap corn, in fact, is the building block of the fast-food nation.  Cheap corn created the chubby 20-ounce bottle of soda we have today.

High fructose corn syrup commonly is 55% fructose and 45% glucose, somewhat different from the 50-50 mix in table sugar, where one fructose molecule is attached to one glucose molecule.  Some HFCS may be as high as 80% fructose.  Since all sugars contain four calories per gram, there must be something else about fructose that matters.  Fructose is metabolized more rapidly that glucose, flooding metabolic pathways and increasing triglyceride storage.   It doesn’t spur the production of insulin or leptin, the hormone that sequesters appetite.  The body then lacks satiety.  This elevates serum triglycerides and increases fat storage.  Since it may have less impact on appetite than glucose, fructose contributes to weight gain.  Ingesting lots of fructose may also reduce insulin sensitivity.  (Beck-Nielsen, 1980)

Soft drink consumption has more than doubled in the twenty years from 1977 to 1997.  Not surprisingly, obesity followed the same trend. Cause and effect? It’s been estimated that for each additional sweet drink consumed per day, the odds of obesity increase by sixty percent.  A study of more than fifty thousand nurses by Harvard compared time periods from 1991-1995 and 1995-1999, and found that women whose soda consumption increased had bigger rises in body-mass index than those who drank less or the same amounts of soda. Fast food seems to go well with it.  Unhealthy foods get along nicely with each other.

The debate between the soft drink industry and the health nuts is ongoing.  People who consume lots of fresh-squeezed juices, vegetables and fruits are not the same group that consumes soda and cold cut sandwiches.  The daily calories from soft drinks account for almost a fourth of the recommended daily intake for many Americans, who drink almost fifty-six gallons of soda a year.

In case you’re interested, more than 30% of Americans are obese. More than 24% of Mexicans, 23% of British, 22% of Slovakians, 22% of Greeks and Australians, 21% of New Zealanders, and 15% of Czechs, but only 3% of Japanese and Koreans. Go figure. Obesity, by the way, means being more than 20% above ideal weight for height.

References

UCLA Health Policy Research Brief
September 2009
Bubbling Over: Soda Consumption and Its Link to Obesity in California
Susan H. Babey, Malia Jones, Hongjian Yu and Harold Goldstein

In California, 62% of adolescents ages 12-17 and 41% of children ages 2-11 drink at least
one soda or other sweetened beverage every day. In addition, 24% of adults drink at least
one soda or other sweetened beverage on an average day. Adults who drink soda occasionally
(not every day) are 15% more likely to be overweight or obese, and adults who drink one or
more sodas per day are 27% more likely to be overweight or obese than adults who do not
drink soda, even when adjusting for poverty status and race/ethnicity.

The prevalence of overweight and obesity has increased dramatically in both adults
and children in the last three decades in the United States. In the 1970s, about 15% of
adults were obese and by 2004 the rate had climbed to 32%.1 Although the prevalence of
overweight among children is lower than among adults, the rates among children and
adolescents have increased considerably more. The prevalence of overweight and obesity
nearly tripled among 12-19 year olds and more than quadrupled among 6-11 year olds
in the last three decades.

In California, 21% of adults are currently obese and an additional 35% are overweight. Among adolescents, 14% are obese and another 16% are overweight.2 Similar to national trends, the trend in California is toward increasing weight in both adults and adolescents.3 Each year in California, overweight and obesity cost families, employers, the health care industry and the government $21 billion.4 California spends more public and private money on the health consequences of obesity than any other state.5

Overweight and obesity are associated with serious health risks. In children and adolescents, overweight and obesity are associated with increased risk for cardiovascular disease indicators including high total cholesterol, high blood pressure, and high fasting insulin, an early indicator of diabetes risk.6 In addition, overweight children and adolescents are more likely to be overweight or obese as adults.7 In adults, overweight and obesity are associated with increased risk for diabetes, heart disease, stroke, some types of cancer and premature death.1, 8, 9

Drinking sweetened beverages such as soda and fruit drinks that have added caloric sweeteners (e.g., sucrose, high fructose corn syrup) is one marker of a poor diet, and is
associated with overweight and obesity in people of all ages.10-13 A number of studies have found that greater consumption of sweetened beverages is associated with overweight and obesity among both adults and children.12-19 In addition, randomized controlled trials that examine the impact of reducing intake of sweetened beverages on weight indicate
that reducing consumption of soda and other sweetened drinks leads to reductions in
overweight and obesity.20, 21 Among adults, drinking soda is also associated with increased risk for type 2 diabetes.13 Moreover, drinking sweetened beverages has
increased, and it is now more common than ever, particularly among adolescents.22
Between 1977 and 2002 Americans increased their calorie intake from soft drinks by
228%.23 Portion sizes have also increased from an average serving size of 6.5 fl oz (88 calories) in the 1950s, to 12 fl oz (150 calories), 20 fl oz (266 calories), and even larger portion sizes common today.24-26 The average serving size of soft drinks in fast food restaurants in 2002 was 23 fl oz (299 calories), with some chains now commonly selling soft drinks in 32 to 64 fl oz portions (416 to 832 calories, respectively).27 Sweetened beverages are a significant contributor to total caloric intake, especially for children and adolescents, and they lack the nutrients our bodies need.24, 26, 28

Additionally, eating habits established in childhood are important determinants of
eating habits as adults.29, 30
http://www.healthpolicy.ucla.edu/pubs/files/Soda%20PB%20FINAL%203-23-09.pdf

SUPPORTING ABSTRACTS
Am J Clin Nutr February 1980 vol. 33 no. 2 273-278
Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects
H Beck-Nielsen, O Pedersen and HO Lindskov

We have studied whether the sucrose-induced reduction of insulin sensitivity and cellular insulin binding in normal man is related to the fructose or the glucose moiety. Seven young healthy subjects were fed their usual diets plus 1000 kcal extra glucose per day and eight young healthy subjects were fed their usual diets with addition of 1000 kcal extra fructose per day. The dietary regimens continued for 1 week. Before change of diet there were no statistically significant differences between body weight and fasting plasma concentrations of glucose, insulin, and ketone bodies in the two groups studied. High- glucose feeding caused no significant changes in insulin binding or insulin sensitivity whereas high-fructose feeding was accompanied by a significant reduction both of insulin binding (P less than 0.05) and insulin sensitivity (P less than 0.05). The changes in insulin binding and insulin sensitivity correlated linearly (r = 0.52, P less than 0.01). We conclude that fructose seems to be responsible for the impaired insulin binding and insulin sensitivity induced by sucrose.

Medscape J Med. 2008;10(8):189. Epub 2008 Aug 12.
Soft drinks and weight gain: how strong is the link?
Wolff E, Dansinger ML.
Boston University School of Medicine, Boston, Massachusetts, USA. [email protected]

CONTEXT
Soft drink consumption in the United States has tripled in recent decades, paralleling the dramatic increases in obesity prevalence. The purpose of this clinical review is to evaluate the extent to which current scientific evidence supports a causal link between sugar-sweetened soft drink consumption and weight gain.

EVIDENCE ACQUISITION
MEDLINE search of articles published in all languages between 1966 and December 2006 containing key words or medical subheadings, such as “soft drinks” and “weight.” Additional articles were obtained by reviewing references of retrieved articles, including a recent systematic review. All reports with cross-sectional, prospective cohort, or clinical trial data in humans were considered.

EVIDENCE SYNTHESIS
Six of 15 cross-sectional and 6 of 10 prospective cohort studies identified statistically significant associations between soft drink consumption and increased body weight. There were 5 clinical trials; the two that involved adolescents indicated that efforts to reduce sugar-sweetened soft drinks slowed weight gain. In adults, 3 small experimental studies suggested that consumption of sugar-sweetened soft drinks caused weight gain; however, no trial in adults was longer than 10 weeks or included more than 41 participants. No trial reported the effects on lipids.

CONCLUSIONS
Although observational studies support the hypothesis that sugar-sweetened soft drinks cause weight gain, a paucity of hypothesis-confirming clinical trial data has left the issue open to debate. Given the magnitude of the public health concern, larger and longer intervention trials should be considered to clarify the specific effects of sugar-sweetened soft drinks on body weight and other cardiovascular risk factors.  PMID: 18924641

Diabetes Care. 2010 Nov;33(11):2477-83. Epub 2010 Aug 6.
Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis.
Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB.

Department of Nutrition, Harvard School of Public Health, and Department of Medicine, Brigham and Women’s Hospital, Boston, MA, USA.

OBJECTIVE
Consumption of sugar-sweetened beverages (SSBs), which include soft drinks, fruit drinks, iced tea, and energy and vitamin water drinks has risen across the globe. Regular consumption of SSBs has been associated with weight gain and risk of overweight and obesity, but the role of SSBs in the development of related chronic metabolic diseases, such as metabolic syndrome and type 2 diabetes, has not been quantitatively reviewed.

RESEARCH DESIGN AND METHODS
We searched the MEDLINE database up to May 2010 for prospective cohort studies of SSB intake and risk of metabolic syndrome and type 2 diabetes. We identified 11 studies (three for metabolic syndrome and eight for type 2 diabetes) for inclusion in a random-effects meta-analysis comparing SSB intake in the highest to lowest quantiles in relation to risk of metabolic syndrome and type 2 diabetes.

RESULTS
Based on data from these studies, including 310,819 participants and 15,043 cases of type 2 diabetes, individuals in the highest quantile of SSB intake (most often 1-2 servings/day) had a 26% greater risk of developing type 2 diabetes than those in the lowest quantile (none or <1 serving/month) (relative risk [RR] 1.26 [95% CI 1.12-1.41]). Among studies evaluating metabolic syndrome, including 19,431 participants and 5,803 cases, the pooled RR was 1.20 [1.02-1.42].

CONCLUSIONS
In addition to weight gain, higher consumption of SSBs is associated with development of metabolic syndrome and type 2 diabetes. These data provide empirical evidence that intake of SSBs should be limited to reduce obesity-related risk of chronic metabolic diseases.

J Public Health Policy. 2004;25(3-4):353-66.
The obesity epidemic in the United States.
Morrill AC, Chinn CD.
Capacities Inc., Watertown, Massachusetts 02471, USA. [email protected]

We describe the epidemic of obesity in the United States: escalating rates of obesity in both adults and children, and why these qualify as an epidemic; disparities in overweight and obesity by race/ethnicity and sex, and the staggering health and economic consequences of obesity. Physical activity contributes to the epidemic as explained by new patterns of physical activity in adults and children. Changing patterns of food consumption, such as rising carbohydrate intake–particularly in the form of soda and other foods containing high fructose corn syrup–also contribute to obesity. We present as a central concept, the food environment–the contexts within which food choices are made–and its contribution to food consumption: the abundance and ubiquity of certain types of foods over others; limited food choices available in certain settings, such as schools; the market economy of the United States that exposes individuals to many marketing/advertising strategies. Advertising tailored to children plays an important role.  PMID: 15683071

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Vitamins? Why?

vitaminsDo you take vitamins? Yes? Why? No? Why not?  Confusing, isn’t it? Can we ever get to the bottom of the yes-no controversy?

First of all, let’s find out what we’re talking about.

The word “vitamins” describes organic substances that are quite diverse in function and structure.  It was initially felt that these compounds could be obtained through a normal diet, and that they were capable of promoting growth and development, and of maintaining life.  The word itself was coined by a Polish biochemist named Casimir Funk, in 1911.  He deemed these substances to be chemical amines, thinking that all contained a nitrogen atom.  Since they were considered to be vital to existence (“vita” means “life” in Latin), they were called “vitamines.”  After it was discovered that they all did not have a nitrogen atom, and, therefore, were not amines, the terminal “e” was dropped.  Funk was working in London at the time, at the Lister Institute, where he isolated a substance without which chickens would suffer neurological inflammation.

The lettered names of the vitamins were ascribed to them in the order of their discovery.  Vitamin K, however, is the exception.  Its label was given by the Danish researcher Henrik Dam, from the word “koagulation.”

If a vitamin is improperly absorbed, or is absent from the diet, a deficiency exists and a specific disease may surface, such as Beriberi, which was noted by William Fletcher in 1905 when symptoms appeared in populations whose diet consisted mostly of polished rice, lacking the thiamine-rich husk.  Lack of thiamine, or vitamin B1, causes emotional disturbances, physical weakness, heart failure, impaired sensory perception, and, in severe circumstances, eventual death.

Scurvy, a deficiency of vitamin C, was once a common ailment of sailors and others who were out to sea for a longer time than their fruits and vegetables could remain edible.  The Latin name of this condition that caused bleeding from the mucus membranes and spongy gums is “scorbutus,” from which we get “ascorbic acid.”  James Lind, a surgeon in the Royal Navy, learned in the 1750s that scurvy could be treated with citrus fruits, and he wrote about his experiments in his 1753 book, “A Treatise of the Scurvy.”

If vitamins are so “vital,” what, exactly, are their roles in human health and well-being?  Vitamin A was first synthesized in 1947, though discovered around 1912 by researchers Elmer McCollum and M. Davis, and later isolated from butter by Yale scientists Thomas Osborne and Lafayette Mendel.  This nutrient contains carotene compounds that are responsible for transmitting light signals to the retina of the eye.  McCollum also uncovered the B vitamins, but later researchers isolated each of the individual factors.

We already know that a lack of B1 causes Beriberi, while a deficiency of B2 may lead to inflammation of the lining of the mouth.  Also called riboflavin, B2 is responsible for the reactions of enzymes, as is its partner, B3 (niacin).  In general, the gamut of B vitamins is involved in the same metabolic processes.  It was decided that a B vitamin must meet specific criteria:  it must be water-soluble, must be essential for all cells, and must function as a coenzyme.  B12 and folate have the added responsibility of being involved in the synthesis of nucleic acid.  Folate is the form of the nutrient naturally found in food, while folic acid is synthetic. Great excesses of one B vitamin can cause deficiencies of the others.  Therefore, if taken as supplements, it is recommended that they be taken together.

Besides preventing scurvy, as mentioned, vitamin C helps the body to make collagen, the protein that acts as the framework for the body.  Collagen is a major component of ligaments and cartilage, it strengthens blood vessels, and it is responsible for skin strength and elasticity.  Vitamin C was the first to be artificially made, in 1935.

Vitamin D is not actually a vitamin, but a prohormone, meaning that it is a precursor to a hormone, called 1,25-D, which helps the body to make its own steroids, such as cholesterol, a substance absolutely necessary to the integrity of each of our trillions of cells.  Vitamin D is needed to maintain correct calcium and phosphorus levels, to assure proper bone mineralization, and to support the immune system.  A severe deficiency leads to rickets, a softening of the bones—usually in children—that was studied in 1922 by Edward Mellanby.

Vitamin E is actually a group of isomers (like-structured molecules) that function as antioxidants.  Study of this fat-soluble nutrient has focused on its purported benefits to the cardiovascular system. University of California researchers discovered vitamin E while studying green, leafy vegetables, in the 1920s.

Another fat-soluble substance, vitamin K is used by the body to assist in the manufacture of bone, and in the manufacture of blood clotting proteins, without which serious bleeding episodes may occur.  This nutrient has been available from green leafy vegetables and from the brassica family, such as broccoli, cauliflower, and kale.

Now the question is, “Can we get all these nutrients from our food, or is supplementation necessary?”

Working at the University of Texas Biochemical Institute, Dr. Donald Davis led a crop-nutrient study in 2004.  He and his team found that the nutrient value of forty-three garden crops has declined considerably over the past fifty years.  As reported in the “Journal of the American College of Nutrition” in December of that year, the forty-three crops showed “statistically reliable declines” in protein, calcium, iron, phosphorus, riboflavin (vitamin B2), and ascorbic acid (vitamin C).  Some nutrients could not be compared because their values were not reported in the 1950s.  They include magnesium, zinc, vitamin B6, vitamin E, dietary fiber, and phytochemicals.

After accounting for possible confounders, the study concluded that the change in nutrient value could be ascribed to changes in cultivated varieties, in which there could have been a trade-off between crop yield and nutrient value.  Dr. Davis added that farmers are paid by the weight of a crop, not by its food value.

Some innovative farming techniques have given rise to faster-growing crops, which, by virtue of their seed-to-market time, do not have sufficient time to develop their nutrients.  They do not have the chance to absorb everything they need from the soil.

Crop rotation has fallen into disfavor by some farms because it requires more planning and management skills than are at hand, thus increasing the complexity of farming.  Rotation of crops helps to reduce insect and disease problems, improves soil fertility, reduces soil erosion, and limits biocide carryover.  If, however, a single crop is a big moneymaker for the farm, why should it bother even to try to grow something else?  Why bother to rotate crops when chemical fertilizers, herbicides, fungicides, and insecticides can help to guarantee a bumper crop?  Could nutrient value be affected by using these artificial chemicals?  Do these materials come into our bodies?  Do we have the proper kinds and amounts of nutrients to detoxify them?  Maybe we do; maybe not.

Nitrogen-fixing bacteria convert atmospheric nitrogen to organic nitrogen, thus contributing to the food value of the crop.  Certain crops, like the legumes, are better than others at replacing nitrogen lost from the soil.  Nitrogen is part of a protein molecule.  Without nitrogen there is no protein.  While it is beneficial to the food and the soil to plant a legume following the harvest of a more lucrative planting, it is not often done.

Therefore, the same plant in place continues to withdraw the same minerals repeatedly, year after year, with little chance for replenishment except by chemical means, if at all.  How many of us would prefer to get our dietary needs from unnatural sources, like iron from rusted nails, or zinc from galvanized wire?

In a study of peaches and pears published in the “Journal of Agriculture and Food Chemistry” in 2002, Marina Carbonaro, of the National Institute for Nutrition Studies, in Rome, reported a difference in the nutrition content of organic versus traditionally raised fruits.  Amounts of polyphenols, citric and ascorbic acids, and alpha-tocopherol were increased in the organically grown crops.  She and her colleagues concluded that the improved antioxidant defense of the plants developed as a result of organic cultivation methods.  Which do you think has more vitamin C?

Here is a sampling of how the nutrient content of broccoli and potatoes sold in Canada has changed from 1951 to 1999.  This information was compiled by Jeffrey Christian.

Broccoli, Raw, 3 spears, 93g. 100/93=1.08
Calcium (mg) Iron
(mg)
Vitamin A (I.U.) Vitamin C (mg) Thiamine (mg) Riboflavin (mg) Niacin (mg)
1951 130.00 1.30 3500 104.0 0.10 0.21 1.10
1972 87.78 0.78 2500 90.0 0.09 0.20 0.78
1999 48.30 0.86 1542 93.5 0.06 0.12 1.07
% Change -62.85 -33.85 -55.94 -10.10 -40.00 -42.86 -2.73
Potatoes, one potato, peeled before boiling, 136g. 100/136=.74
Calcium (mg) Iron
(mg)
Vitamin A (I.U.) Vitamin C (mg) Thiamine (mg) Riboflavin (mg) Niacin (mg)
1951 11.00 0.70 20.00 17.00 0.11 0.04 1.20
1972 5.74 0.49 0.00 16.39 0.09 0.03 1.15
1999 7.97 0.30 0.00 7.25 0.09 0.02 1.74

The USDA, in its statistical bulletin # 978, made public in June, 2002, titled “The Changing Landscape of U. S. Milk Production,” admitted that milk production has increased because of “advances in animal nutrition and health, improved artificial breeding techniques, and the recent addition of biotechnology, such as…rbST…”
rbST is a hormone that is administered to cows to increase milk production.  Take a look at how milk production has changed, and then decide if there might be implications that could involve humans.

In 1950, a single cow (I mean one cow, not an unmarried cow.) produced 5,314 pounds of milk.  By 1975, she increased her output to 10,360 pounds.  In 2000, that amount increased to 18,204 pounds.  The USDA admits that “…a 76-percent increase in milk per cow since 1975 is substantial.”  Substantial?  How about phenomenal, even miraculous?  Could a factory have increased its output by seventy-five percent in twenty-five years?  Could a weight lifter elevate that much of a weight increase in a military press as he did twenty-five years ago?  Could recombinant bovine somatotropin enter the milk supply and affect human growth and development, or even contribute to human misery?

Not only do modern agricultural techniques affect the quality of food, but also do the processes by which food is processed and packaged.  To prevent the growth of pathogenic bacteria, some canned foods are exposed to temperatures that compromise their nutritional value.  Acidic foods, like tomatoes, are excused from excessive heat because their nature does not support the growth of food poisoning bacteria.  Others are heated to temperatures high enough to destroy bacteria, yeasts, and molds that could cause foods to spoil.  Heating to 250 degrees Fahrenheit for three minutes not only kills pathogens, but also denigrates the potency of water-soluble vitamins.  If these foods are consumed without also consuming the water in which they are prepared, nutrition is sacrificed.

The USDA has a table of nutrient retention factors that compare the nutritional value of processed foods.  This table includes most nutrients from alpha-tocopherol to zinc.  It is noted that folate, for example, a nutrient easily lost in food preservation and preparation, is diminished by almost 50% in canned fruits as compared to fresh and frozen.  Additionally, canned foods are higher in sodium, and their texture is softer than either fresh or frozen.  The mineral and protein values of canned foods are usually undisturbed.  In rare instances, as with tomatoes and pumpkin, nutrient value is retained, or even increased, by canning.  We should note that canned fruits and vegetables are better than none at all.

Frozen foods, on the other hand, retain much of the nutrition they are destined to have.  The folate retention factor for frozen fruits is ninety-five, contrasted to fifty for canned.  There are some compromises, though, because frozen foods need to be blanched prior to being frozen.  Blanching, however, is no worse than what happens to foods during normal cooking activity.  This means that frozen vegetables provide levels of nutrition similar to fresh, provided they are stored and handled properly.  The “International Journal of Food Science and Technology,” reported in June of 2007 that the freezing process alone does not affect vitamin levels, but that the initial processing and later storage do.  About 25% of vitamin C and a higher percentage of folate are lost through the blanching process.  These numbers will vary according to the processing techniques.

An advantage to canned and frozen foods is that the foods themselves are harvested at their maximum stage of development, containing all the vitamins and minerals they could possibly extract from their environments.  What we call “fresh” vegetables are usually anything but.  They have been picked before their maximum ripeness so that they can be shipped across the country.  If not harvested locally, “fresh” vegetables are more accurately labeled as “raw,” or “unprocessed.”  Water-soluble vitamins, like the B complex and vitamin C, are affected by exposure to light and air.  Vitamin A is jeopardized by exposure to light, as well.  The amount of time that a raw vegetable spends in storage may take its toll on nutrient integrity, also.

Typical Maximum Nutrient Losses (as compared to raw food)
Vitamins Freeze Dry Cook Cook+Drain Reheat
Vitamin A 5% 50% 25% 35% 10%
  Retinol Activity Equivalent 5% 50% 25% 35% 10%
  Alpha Carotene 5% 50% 25% 35% 10%
  Beta Carotene 5% 50% 25% 35% 10%
  Beta Cryptoxanthin 5% 50% 25% 35% 10%
  Lycopene 5% 50% 25% 35% 10%
  Lutein+Zeaxanthin 5% 50% 25% 35% 10%
Vitamin C 30% 80% 50% 75% 50%
Thiamin 5% 30% 55% 70% 40%
Riboflavin 0% 10% 25% 45% 5%
Niacin 0% 10% 40% 55% 5%
Vitamin B6 0% 10% 50% 65% 45%
Folate 5% 50% 70% 75% 30%
  Food Folate 5% 50% 70% 75% 30%
  Folic Acid 5% 50% 70% 75% 30%
Vitamin B12 0% 0% 45% 50% 45%
Minerals Freeze Dry Cook Cook+Drain Reheat
Calcium 5% 0% 20% 25% 0%
Iron 0% 0% 35% 40% 0%
Magnesium 0% 0% 25% 40% 0%
Phosphorus 0% 0% 25% 35% 0%
Potassium 10% 0% 30% 70% 0%
Sodium 0% 0% 25% 55% 0%
Zinc 0% 0% 25% 25% 0%
Copper 10% 0% 40% 45% 0%

Can we get all the vitamins and minerals we need from food?  No.

Take a look at vitamin C, one of the most-studied nutrients.  Because of its fragile nature, vitamin C, a popular water-soluble supplement, needs special handling.  This characteristic may explain why it seems to have been a major focus of the food business for years.  It is extremely sensitive to heat, and slightly less so to light, and time.  Loss of vitamin C during processing ranges from about 10% in beets to almost 90% in carrots.  The amount of vitamin C at the start has no bearing on the outcome.  It’s the percentage that makes the matter a real concern.  Since this vitamin is easily oxidized, it is difficult to measure levels in drained liquids.  That goes for the cooking water, as well.  Canned foods are further insulted by cooking at high temperatures for a long time, without a lid.  It is nutritionally prudent to include the water from the can in the meal.  Otherwise, the ascorbic acid goes down the drain.  The table below demonstrates changes in vitamin C levels resulting from canning alone.

Ascorbic acid (g / kg−1 wet weight) in fresh and canned vegetables
Commodity Fresh Canned % Loss
Broccoli 1.12 0.18 84
Corn 0.042 0.032 0.25
Carrots 0.041 0.005 88
Green peas 0.40 0.096 73
Spinach 0.281 0.143 62
Green beans 0.163 0.048 63
Beets 0.148 0.132 10
J Sci Food Agric 87:930–944 (2007) Nutritional comparison of fresh, frozen and canned fruits and vegetables. Part 1. Vitamins C and B and phenolic compounds. Joy C Rickman, Diane M Barrett and Christine M Bruhn

 Freezing has less impact on nutrient levels than other types of processing. Because foods are harvested at their maximum maturity stage before freezing, they already contain the most nutritive value they can be expected to have. The table that follows shows losses of ascorbic acid (vitamin C) after periods of storage at various temperatures, starting at room temperature (20° C; 68° F), through the refrigerator crisper drawer (4° C; 39° F), to the freezer (-20° C; -4° F).

Losses of ascorbic acid (% dry weight) due to fresh and frozen storage
Commodity Fresh, 20 ◦C,
7 Days
Fresh, 4 ◦C,
7 Days
Frozen, −20 ◦C,
12 Months
Broccoli 56 0 10
Carrots 27 10
Green beans 55 77 20
Green peas 60 15 10
Spinach 100 75 30
J Sci Food Agric 87:930–944 (2007) Nutritional comparison of fresh, frozen and canned fruits and vegetables. Part 1. Vitamins C and B and phenolic compounds. Joy C Rickman, Diane M Barrett and Christine M Bruhn

Vitamin C does continue to degrade after long periods of freezing, but at a slower rate. What seems to be the main factor in this process is the moisture content of the food at the outset. Notice that refrigerating foods as soon as they come home from the market plays a serious role in maintaining nutritive value. The cook is the penultimate figure in the saga of a food’s life. The method of cooking can cause loss of ascorbic acid at the rate of 15% to 55%. Losses in canned products are probably minimal because the food already sits in water. Oddly, unheated canned products are occasionally comparable to that which is cooked fresh. But who has the wherewithal to determine that at home? Remember that, because vitamin C oxidizes in air, the value of frozen foods may be substantially higher than fresh foods that have been stored for a long time or under sub-optimal conditions. So…fresh (raw) may not always be the best. Whatever the case, additional research is expected to substantiate changes in vitamin C levels caused by cooking habits. Microwaving, for example, may have an unexpected influence, based on the solubility and diffusion of certain food solids, such as sugars that may diminish faster than ascorbic acid, leaving vitamin C behind.

It is necessary to realize that carrots are not exactly heralded for their vitamin C value in the first place, so losses are relatively insignificant. Also, note that sources of information may present nonconcurring results due to variations in measurement techniques, quality of raw ingredients, and other variables.

The water-soluble B vitamins (all are water-soluble) suffer a fate similar to that of ascorbic acid. Thiamin, the least stable of the vitamins to thermal indignity, is most sensitive to degradation caused by food processing. But, since fruits and vegetables are not exceptional sources of this nutrient, its retention or loss does not represent overall nutrient retention or loss of a particular food. Riboflavin is unstable in the presence of light. Processing and storage / display play a role in its stability. Clear glass containers can cause this vitamin to dwindle. Realization of this fact by the food industry is one reason that certain foods are now in opaque containers. The exception to the B-vitamin family is vitamin B12 because it is found mostly in animal products. The same considerations that apply to vitamin C are appropriate for the B vitamins.

The normal eating habits of Americans suggest that we are woefully inadequate in meeting dietary recommendations to achieve optimum well-being and health.  Most of us do not eat the recommended number of daily servings of fruits and vegetables.  For some nutrients, daily intake needs may be higher for some populations than for others, especially those in particularly vulnerable groups, such as those with gastrointestinal problems or poor absorption, those who are chronically ill, those who are alcohol or drug dependent, and the elderly.

The June 19, 2002 edition of the “Journal of the American Medical Association” recanted that august body’s negative position on vitamin supplements when it advised all adults to take at least one multivitamin tablet a day.  The article, “Vitamins for Chronic Disease Prevention in Adults,” authored by Robert H. Fletcher, MD, MSc, and others, agreed that suboptimal levels of folic acid and vitamins B6 and B12 are a risk factor for cardiovascular disease, neural tube defects, and colon and breast cancers.  It added that risks for other chronic diseases are increased by low levels of the antioxidant vitamins A, C, and E.

Because it is accepted that high homocysteine levels are associated with increased risk of heart disease, the AMA’s recommendation for optimal levels of cardio-specific supplements are well founded.

Depending on a person’s physiological state, he or she may need more of a particular nutrient than is available from a multivitamin alone.  The bioavailability of a specific nutrient from a high quality supplement is close to one hundred percent, compared to a food whose life experiences might have been less than ideal.  In a society that falls short of consuming the five to nine servings of fruits and vegetables that are recommended, it would be inane to ask them to eat more fruits and vegetables to get the nutrients they lack.

This does not mean that a person should take a little of this and a little of that because he read about it somewhere.  On the contrary, supplementation with vitamins, minerals, and herbs is a scientific enterprise that entails one’s medical history, both distant and recent past, one’s current physiological state, and even one’s blood chemistry.

Do you take vitamins?

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Sunflower Seeds Lower Cholesterol

plant sterols and stanolsSunflower seeds and pistachio nuts are top snacks for reducing cholesterol. Scientists have known for a long time that nuts and seeds are rich sources of phytosterols, plant compounds that are structurally related to cholesterol and may lower LDL levels. Keeping cholesterol in check may be your goal, but it’s not realistic to accomplish this without some work…as in exercise.

It’s been a few years since Science Daily first reported the news that chemists at Virginia Polytechnic Institute found the plant sterols in pistachios and sunflowers seeds to be valuable assets in the fight against rampant cholesterol numbers.  (ScienceDaily, 7 Dec. 2005. Web. 19 Aug. 2011.)  “Sesame seed and wheat germ had the highest total phytosterol content and Brazil nuts the lowest,” said scientists at VPI. (Phillips. 2005)  But these are not typically consumed as snack foods.  Sunflower seeds and pistachio nuts, on the other hand, are, and were found to be richest in these compounds.

Dietary phytosterols favorably alter cholesterol metabolism in a dose-dependent manner by reducing intestinal cholesterol absorption.  (Racette. 2010)  Even a moderate intake can be obtained from a healthy diet, without supplementation.  Of course, you have to eat the right foods.  Plants contain a large range of phytosterols, which are structural components of the cell wall.  (Plants have cell walls and cell membranes; animals just the membrane.)  What phytosterols do for plants, cholesterol does for animals.

As functional foods, plant sterols and stanols demonstrate a strong lipid-lowering effect. (Moore. 2011)  Including them as part of the diet may reduce risk for heart disease.  Studies at McGill University concentrated on patients with Type 2 diabetes and found that plant sterols had a significantly more profound effect on the cholesterol levels of Type 2 patients than on patients with high cholesterol without diabetes. (Lau. 2005)  LDL levels were lowered while the desirable HDL was relatively untouched.  Additional lipid study in Israel learned that consuming plant sterols also results in a drop in circulating insulin levels, pointing to their use as food enhancers that can reverse insulin resistance and hyperlipidemia, and possible help to control body weight.  (Ziv. 2009)

Controlling lipid levels with food or supplements is considerably more desirable than using drugs.  Suggested intake of two to three grams of these plant compounds a day, either from food, fortified foods, or supplements, can reduce lipids by almost ten percent.  (Baumgartner. 2011)  More than that affords no increased benefit.

Whether raw or roasted, sunflower seeds have a dedicated following.  Because they’re high in oil, the seeds are prone to rancidity, so refrigeration is a good idea.  They aren’t just for snacks, either.  They match pretty well with all the food groups and can really up the ante on nutrition.  Sauté them with vegetables, add them to your salads, fold them into meatloaf and mix them with baked goods and even eggs.  An ounce will give you two grams of fiber, almost half a day’s vitamin E, and a healthy ration of minerals.

References

American Chemical Society.
Sunflower Seeds, Pistachios Among Top Nuts For Lowering Cholesterol.
ScienceDaily, 7 Dec. 2005. Web. 19 Aug. 2011.

J. Agric. Food Chem., 2005, 53 (24), pp 9436–9445
Phytosterol Composition of Nuts and Seeds Commonly Consumed in the United States
Katherine M. Phillips, David M. Ruggio, and Mehdi Ashraf-Khorassani

Am J Clin Nutr January 2010 vol. 91 no. 1 32-38
Dose effects of dietary phytosterols on cholesterol metabolism: a controlled feeding study
Susan B Racette, Xiaobo Lin, Michael Lefevre, Catherine Anderson Spearie, Marlene M Most, Lina Ma, and Richard E Ostlund Jr

Curr Opin Endocrinol Diabetes Obes. 2011 Aug 11. [Epub ahead of print]
Functional foods and cardiovascular disease risk: building the evidence base.
Moore LL.

Am J Clin Nutr June 2005 vol. 81 no. 6 1351-1358
Plant sterols are efficacious in lowering plasma LDL and non-HDL cholesterol in hypercholesterolemic type 2 diabetic and nondiabetic persons
Vivian WY Lau, Mélanie Journoud and Peter JH Jones

Lipids Health Dis. 2009 Oct 12;8:42.
A high oleic sunflower oil fatty acid esters of plant sterols mixed with dietary diacylglycerol reduces plasma insulin and body fat accumulation in Psammomys obesus.
Ziv E, Patlas N, Kalman R, Pelled D, Herzog Y, Dror T, Cohen T.

Curr Pharm Des. 2011;17(9):922-32.
Plant sterols and stanols in the treatment of dyslipidemia: new insights into targets and mechanisms related to cardiovascular risk.
Baumgartner S, Mensink RP, Plat J.
Department of Human Biology, School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, The Netherlands.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

USDA vs Healthy Eating

food-pyramid-on-plateThe food pyramids and plates conjured up by the USDA haven’t quite lived up to their expectations. In its attempts to get it right, this august, though somewhat misguided, body has delivered several versions, each one anticipated to be new and improved. So far, none has panned out.

The most visible sign of U.S. nutrition policy is the Food Pyramid, or lately, the Food Plate.  Recognizing that dietary quality plays a role in health and the prevention of chronic disease, the USDA issued a Pyramid revision in 2005 to address the shortcomings of the previous one.  Walter Willett, chair of Harvard’s nutrition department, comments, “…the previous pyramid was in substantial discordance with current scientific evidence.”   If such a guideline is out of harmony with what research concludes to be so, then a critical eye needs to be cast at the base of its formulation.  Willett adds that, “My Pyramid strays from much of the evidence generated through years of research and, in our opinion, fails to provide the public with clear information about healthy food choices.”  (Chiuve. 2007)

The older Food Pyramid had so many carbohydrates at its base that you could have made wallpaper paste for all your friends.  The bread, cereal, rice and pasta food group didn’t mention any difference between refined and whole grains.  Not that it makes much difference, since they’ll spike your insulin, anyhow, with high glycemic factors and initiate metabolic and hyperlipidemic aberrations, including insulin resistance, a precursor to Type 2 diabetes.  The newer 2005 Food Pyramid, with vertical lines instead of horizontal groups, is not only hard to fathom, but also vague.  However, it does mention whole grains.  In June, 2011, with lots of hoopla, the USDA replaced the much-maligned-but-deserving-of-it My Pyramid with a simpler icon, the fruit and vegetable-festooned My Plate.

It needs to be realized that the Department of Agriculture is not in the business of promoting health.  Its job is to promote farmers and foods.  Therefore, your hunt for sage dietary counsel has to travel another direction.  What’s good about the new My Plate is that the flawed My Pyramid has been dismantled.  What’s not so good about My Plate is its misplay in providing all the nutrition advice you need to choose the healthiest diet.  Picky?  Why not?  Who’s paying the freight?

The sections of My Plate don’t give us all the dope we need to make good food choices.  For one thing, it forgets to tell the shopper that whole grains are better for health, since refined grains can contribute to weight gain and elevated triglycerides.
(Hudgins. 2000)  (Parks.  2001)  It also fails to say that all proteins are not created equal.  Some are better for us than others because they have less saturated fat and, like fish, more polyunsaturated essential fats.  Processed meats are harmful to health.  That includes the ubiquitous hot dog.  How about beans and nuts as protein sources?  Good choices.  A hot dog or hamburger on a white-bread bun with fries and a shake can be part of the My Plate cuisine…despite the fact that high red meat and processed meat intake can increase risk for disease.  (Pan. 2011)  (Bernstein. 2010)

My Plate doesn’t distinguish between potatoes and other vegetables.  Potatoes are loaded with rapidly digested starch, having the same effect on blood sugar as refined grains and sweets.  (Hu. 2009)  Sadly, My Plate is silent about fats—the healthy fats, the essential fats.  The good fats can keep cholesterol under control…and the rest of the lipid panel, for that matter.  (Bester. 2010)

The topic of dairy can polarize a community.  Even though it contains a foreign protein, is a poor distributor of calcium, and is allowed to carry a percentage of bovine somatic cells, dairy has its following.  In fact, there is little solid evidence that high dairy intake prevents osteoporosis, but to the contrary, that the countries consuming the most dairy have the highest rates.  (Feskanich. 1997)  (Cumming. 1994)  My Plate recommends dairy at every meal.  It includes nothing about sugary drinks and fiberless juices.

What to do?  For starters, Dr. Willett relates, “If Americans could eliminate sugary beverages, potatoes, white bread, pasta, white rice and sugary snacks, we would wipe out almost all the problems we have with weight and diabetes and other metabolic diseases.”  His colleague, Dr. Frank Hu, admits that, “The country’s big low-fat message backfired.  The overemphasis on reducing fat caused the consumption of carbohydrates and sugars to soar.  The shift may be linked to the biggest health problems in America today.”  (LA Times. 2010)  For a better food plate, check out Harvard School of Public Health, at http://www.hsph.harvard.edu/nutritionsource/  Then swap carbohydrate and fat percentages in your daily intake.

References

Chiuve SE, Willett WC. The 2005
Food Guide Pyramid: an opportunity lost?
Nat Clin Pract Cardiovasc Med. 2007 Nov;4(11):610-20.

Hudgins LC.
Effect of high-carbohydrate feeding on triglyceride and saturated fatty acid synthesis.
Proc Soc Exp Biol Med. 2000 Dec;225(3):178-83.

Parks EJ.
Effect of dietary carbohydrate on triglyceride metabolism in humans.
J Nutr. 2001 Oct;131(10):2772S-2774S.

Pan A, Sun Q, Bernstein AM, Schulze MB, Manson JE, Willett WC, Hu FB.
Red meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis
Am J Clin Nutr. 2011 Aug 10.

Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC.
Major dietary protein sources and risk of coronary heart disease in women.
Circulation. 2010 Aug 31;122(9):876-83.

Hu Y, Block G, Sternfeld B, Sowers M.
Dietary glycemic load, glycemic index, and associated factors in a multiethnic cohort of midlife women.
J Am Coll Nutr. 2009 Dec;28(6):636-47.

Bester D, Esterhuyse AJ, Truter EJ, van Rooyen J.
Cardiovascular effects of edible oils: a comparison between four popular edible oils.
Nutr Res Rev. 2010 Dec;23(2):334-48.

Feskanich D, Willett WC, Stampfer MJ, Colditz GA.
Milk, dietary calcium, and bone fractures in women: a 12-year prospective study.
Am J Public Health. 1997 Jun;87(6):992-7.

Cumming RG, Klineberg RJ.
Case-control study of risk factors for hip fractures in the elderly.
Am J Epidemiol. 1994 Mar 1;139(5):493-503.

Harvard School of Public Health
The Nutrition Source
http://www.hsph.harvard.edu/nutritionsource/

Marni Jameson
A reversal on carbs: Fat was once the devil. Now more nutritionists are pointing accusingly at sugar and refined grains.
Los Angeles Times.  December 20, 2010
http://articles.latimes.com/2010/dec/20/health/la-he-carbs-20101220

Dina Fitzsimons
Why Milk Won’t Prevent Osteoporosis-And The Protein Myth-
https://www.msu.edu/~corcora5/food/vegan/osteo.html

Harvard School of Public Health
The Nutrition Source
Calcium and Milk: What’s Best for Your Bones and Health?
http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/calcium-full-story/

Belin RJ, Greenland P, Allison M, Martin L, et al
Diet quality and the risk of cardiovascular disease: the Women’s Health Initiative (WHI).
Am J Clin Nutr. 2011 Jul;94(1):49-57.

Am J Clin Nutr. 2011 Jul;94(1):247-53. Epub 2011 May 25.
Alternative Healthy Eating Index and mortality over 18 y of follow-up: results from the Whitehall II cohort.
Akbaraly TN, Ferrie JE, Berr C, Brunner EJ, Head J, Marmot MG, et al

Willett WC, McCullough ML.
Dietary pattern analysis for the evaluation of dietary guidelines.
Asia Pac J Clin Nutr. 2008;17 Suppl 1:75-8.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Protein Zaps Belly Fat

abdomenIn a sedentary, over-fed, yet undernourished society, the dissolution of abdominal fat with a magic bullet is an incessant quest.  First, we cut out the junk food.  Then we try to eat a balanced diet, the definition of which seems elusive.  After that, we add the foods we think are good for us.  Still, we can’t burn the belly.  Next, we look closer at the ads for products guaranteed to get rid of excess adiposity.  Only after these promises fail do we notice the small print that says the results you see are not typical, and that it must be accompanied by diet and exercise.  Oh, no, I have to work at it.  What happened to the magic bullet?

To be realistic about losing fat, we have to do something actively, not passively.  But that might be as simple as upping the ante on protein.  However, it just isn’t plain, old protein, but the quality of the protein that makes the difference.  Actually it’s the amino acids, the protein building blocks whose chemical properties determine the biological activity of the proteins of which they are a constituent.   Proteins catalyze many of the reactions in living cells—enzymes, hormones, antibodies.  The folding of proteins into three dimensional structures depends upon the information in the amino acid sequences.  Although several hundred kinds of amino acids have been found in nature, only twenty or so apply to human peptides (two or more aminos joined together) and proteins.  Low levels of certain amino acids telegraph as specific problems that include hormone imbalances, lack of concentration, irritability, and even depression.

Based on their individual characteristics, amino acids may be classified as essential, non-essential, or conditionally essential.  Essentiality does not bespeak importance, but acquisition.  The essential ones need to be acquired from diet because they can’t be made by the body.  Here’s a quick rundown of the essential amino acids, with some of their features:

Leucine — a BCAA (branched chain amino), is used for tissue repair after surgery, to build muscle mass, to balance blood sugar, to de-stress, to manufacture HGH (human growth hormone), and for protein synthesis.  It helps to maintain healthy bone, skin, and hemoglobin.

Isoleucine — a BCAA (branched chain amino), addresses mental disorders, tissue rebuild after surgery, energy, muscle, endurance, and blood hemoglobin.

Valine — a BCAA (branched chain amino), is used for mental and emotional disorders, for glycogen production, and in alcohol and drug recovery.  It’s used in muscle metabolism, where it contributes to the structure of proteins.

Lysine — absorbs and conserves calcium and maintains nitrogen balance.  It helps to make collagen, to manage cholesterol and triglycerides, and bolsters the immune system.  (People use this for fever blisters.)

Methionine — has been used to address schizophrenia, and the muscle weakness of Parkinson’s.  It helps to detoxify heavy metals, to form collagen, to prevent brittle hair and nails, to protect against radiation toxicity, and to control histamine levels that may affect cognitions.  Additionally, methionine is a strong antioxidant.

Phenylalanine — addresses chronic pain, helps to make endorphins, assists the manufacture of norepinephrine to direct nerve signals in the brain, promotes alertness and elevates mood, and has been used to treat arthritis, depression, migraines, and Parkinson’s disease.

Threonine — helps to maintain proper protein balance, is important to collagen, elastin, and tooth enamel, aids wound healing, may prevent fatty liver, and assists assimilation.

Tryptophan — is a natural relaxant that helps to alleviate insomnia.  It stabilizes mood, fights migraines and fibromyalgia, and may aid in weight control by reducing appetite.

Histidine — is conditional in adults, but deemed essential to infants and children, and is the immediate precursor to histamine (and carnosine).  Histidine is abundant in hemoglobin, and has been used in the treatment of arthritis, gastric disorders, and the maintenance of the myelin sheath.  It protects against heavy metals and radiation, and aids in the manufacture of red and white blood cells.

The remaining amino acids are non-essential, and are produced from the breakdown of proteins or from the essential ones.  They and a few of their jobs are:

Alanine — (the other component of carnosine) transfers nitrogen from peripheral tissue to the liver in glucose metabolism and guards against the buildup of toxins when muscle tissue is broken down to meet energy needs, as occurs in serious aerobic exercise.

Arginine — is considered the natural Viagra, relaxes blood vessels, supports thymus immunity activity, helps to neutralize ammonia, assists the release of growth hormones, and stimulates the pancreas to release insulin.

Aspartic Acid — from asparagine, is used to treat chronic fatigue and depression, aids the elimination of ammonia, rejuvenates cell activity, and helps to move minerals across the intestinal lining into the bloodstream.

Cysteine — (and cysteine) works as a potent antioxidant and protects against radiation and the toxins of tobacco smoke.  It promotes recovery from burns and promotes the burning of fats. Cystine is formed from the oxidation of two cysteines, but has the same character and activity.

Glutamic Acid — is an excitatory neurotransmitter that is called glutamine after coupling with ammonia, which is carried to the liver for disposal.  Free glutamic acid is important to the metabolism of fats and sugars, and helps to carry potassium into spinal fluid.

Glutamine — is structurally akin to glutamic acid.  It’s the most abundant amino found in muscles, which it helps to build and maintain, where it is useful for those confined to bed for long periods.  It helps to maintain acid-alkaline balance, and might be able to reduce cravings for sugar and alcohol.

Glycine — participates in the biosynthesis of hemoglobin, improves glycogen storage, and is part of the purine component of genetic material.

Ornithine — could be classed with “other” amino acids, helps to release growth hormones, which promotes the metabolism of excess body fat.  It detoxifies ammonia and may help insulin to function as an anabolic agent.  It’s formed from arginine.

Proline — improves skin texture via formation and salvation of collagen.  It works with vitamin C to promote healthy connective tissues.

Serine — is needed for the metabolism of fats and fatty acids, and for participation in the biosynthesis of genetic compounds important to RNA and DNA.

Taurine — is also among the “others.”  It boosts the heart muscle and vision, where it helps to deal with macular degeneration.  Taurine is a key component of bile, and may prevent cardiac arrhythmia.

Tyrosine — is important to overall metabolism, and is a precursor to norepinephrine and dopamine, which regulate mood.  It may suppress appetite and helps to reduce body fat.  Tyrosine affects thyroid hormones.

In a weight management study described in the January, 2012, issue of Nutrition and Metabolism, researchers were able to determine a relationship between the amount of quality protein ingested and central abdominal fat.  They especially paid attention to the number of times that approximately ten grams of essential amino acids (EAA) were consumed in a meal.  Noting that the dietary reference intake (DRI) has no specific recommendations for the types of dietary protein consumed or the distribution of protein throughout the day (Layman, 2009) (Drewnowski, 2001), these scientists drew their conclusion based on maximal stimulation of muscle protein synthesis, thereby arriving at the ~10 gram level, adding that greater amounts do not improve the outcome. (Loenneke, 2012)

Calculating the amount of essential amino acids (EAA) in a meal requires more labor than many of us are able or willing to perform, mostly because we lack the immediate resources needed to find out the base levels of each food in the meal.  There are books and websites that can help with this venture if you are so inclined.  However, eating a quality protein at each meal should do the job.  That usually includes meat, fish, eggs, and dairy, which are complete proteins, meaning that they have all the essential amino acids.   (Egg whites are excellent protein foods.)  Because grains and nuts lack lysine, and legumes lack methionine, it’s a good idea to combine them, as in rice and beans.  Combining essential aminos is not necessary at every meal, but it is in the course of the day.

Whey protein has been shown to stimulate a considerable rise in muscle protein synthesis and results in greater muscle cross-sectional area, especially if combined with a little resistance training—and it enhances recovery after exercise.  (Hulmi, 2010)  Older people show a decreased anabolic sensitivity to essential amino acids, probably because of declining intramuscular expression and receptor activation that are associated with slower anabolic signaling.  (Cuthbertson, 2005)   Among the countermeasures under investigation is regular resistance exercise, regardless of intensity or duration.  In physiological studies at the U. of TX, it was found that the only difference between young and old is the rapidity of the positive response to EAA’s.  (Drummond, 2008)  Timing of EAA ingestion for exercisers makes a difference.  Consume them afterwards.

Stimulating muscle protein synthesis is important to body composition.  If you multiply your body weight in kilograms (2.2 pounds) by 0.8, you’ll arrive at the number of grams of protein you need every day.  (You could also multiply pounds by 0.37.  Why didn’t we say that in the first place?)  More than 30 grams of protein in a single meal does not enhance protein synthesis.  This translates that 113 grams (about 4 oz.) of beef is enough, at 220 calories and 30 grams of protein.  (Symons, 2009)  Therefore, that 12-ounce steak from your favorite eatery isn’t doing much more than filling you up.  While you’re at that restaurant, skip the simple carbs if you’re looking to lose a few inches.  There’s a positive association between girth and consumption of potatoes, refined grains (including alcohol) and simple sugars, but a negative association with protein.  (Halkjaer, 2006)

Protein intake has added benefit—satiety.  If you feel full longer, you’ll eat less and, therefore, consume fewer calories.  Protein increases satiety to a greater degree than fats or carbohydrates (although fats beat carbs), and higher-protein diets result in thermogenesis, which augments energy expenditure.  And, if you have high triglycerides (from eating too many refined and starchy carbohydrates), complete protein is able to attenuate that while you change body composition to something more desirable.  (Clifton, 2009)  (Clifton, 2008)  Don’t forget to choose lean protein, to remove visible fat from your steaks and the skin from poultry, and to add legumes to your regimen.

References

Clifton PM, Keogh JB, Noakes M.
Long-term effects of a high-protein weight-loss diet.
Am J Clin Nutr. 2008 Jan;87(1):23-9.

Clifton PM, Bastiaans K, Keogh JB.
High protein diets decrease total and abdominal fat and improve CVD risk profile in overweight and obese men and women with elevated triacylglycerol.
Nutr Metab Cardiovasc Dis. 2009 Oct;19(8):548-54.

Cuthbertson D, Smith K, Babraj J, Leese G, Waddell T, Atherton P, Wackerhage H, Taylor PM, Rennie MJ.
Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle.
FASEB J. 2005 Mar;19(3):422-4.

Drewnowski A, Warren-Mears VA.
Does aging change nutrition requirements?
J Nutr Health Aging. 2001;5(2):70-4.

Drummond MJ, Dreyer HC, Pennings B, Fry CS, Dhanani S, Dillon EL, Sheffield-Moore M, Volpi E, Rasmussen BB.
Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging.
J Appl Physiol. 2008 May;104(5):1452-61.

Fujita S, Dreyer HC, Drummond MJ, Glynn EL, Volpi E, Rasmussen BB.
Essential amino acid and carbohydrate ingestion before resistance exercise does not enhance postexercise muscle protein synthesis.
J Appl Physiol. 2009 May;106(5):1730-9.

Halkjaer J, Tjønneland A, Thomsen BL, Overvad K, Sørensen TI.
Intake of macronutrients as predictors of 5-y changes in waist circumference.
Am J Clin Nutr. 2006 Oct;84(4):789-97.

Hulmi JJ, Lockwood CM, Stout JR.
Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein.
Nutr Metab (Lond). 2010 Jun 17;7:51.

Layman DK.
Dietary Guidelines should reflect new understandings about adult protein needs.
Nutr Metab (Lond). 2009 Mar 13;6:12.

Loenneke JP, Balapur A, Thrower AD, Syler G, Timlin M, Pujol TJ.
Short report: Relationship between quality protein, lean mass and bone health.
Ann Nutr Metab. 2010;57(3-4):219-20.

Loenneke JP, Wilson JM, Manninen AH, Wray ME, Barnes JT and Pujol TJ
Quality protein intake is inversely associated with abdominal fat
Nutrition and Metabolism.  Jan, 2012; 9:5

Paddon-Jones D, Westman E, Mattes RD, Wolfe RR, Astrup A, Westerterp-Plantenga M.
Protein, weight management, and satiety.
Am J Clin Nutr. 2008 May;87(5):1558S-1561S.

Sites CK, Cooper BC, Toth MJ, Gastaldelli A, Arabshahi A, Barnes S.
Effect of a daily supplement of soy protein on body composition and insulin secretion in postmenopausal women.
Fertil Steril. 2007 Dec;88(6):1609-17.

Symons TB, Sheffield-Moore M, Wolfe RR, Paddon-Jones D.
A moderate serving of high-quality protein maximally stimulates skeletal muscle protein synthesis in young and elderly subjects.
J Am Diet Assoc. 2009 Sep;109(9):1582-6.

Tipton KD, Gurkin BE, Matin S, Wolfe RR.
Nonessential amino acids are not necessary to stimulate net muscle protein synthesis in healthy volunteers.
J Nutr Biochem. 1999 Feb;10(2):89-95.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Low Cholesterol And Mental Health

sad-eggsIf mental health is defined as a state of emotional and psychological well-being in which an individual is able to use his or her cognitive and emotional capabilities, function in society, and meet the ordinary demands of everyday life, then we need to take care of the garage in which this vehicle is kept.  Measures of depression and anxiety assess things such as self-disparagement, pessimism, lack of drive, apprehension, inability to relax, and irritability, to name a few.  Interestingly, these evaluations have demonstrated a relationship to low lipid and lipoprotein concentrations.

In work done at the end of the last century, an inverse association between mental challenges and total cholesterol and lipids was found.  That means when one goes up, the other goes down.  Testing young adult females, Duke University Medical Center discovered that women “…with low total cholesterol concentrations (<4.14 mmol/liter) relative to those with moderate to high cholesterol levels, were more likely to have higher scores on the NEO depression subscale…and anxiety subscale…” after adjustments were made for age, body mass index, oral contraceptive use and physical activity.  (Suarez.  1999)

Before we got too involved, it pays to know that 4.14 mmol/liter is equal to a cholesterol level of 160 mg/dL, or just plain 160.  Cholesterol is a steroid substance necessary to human life.  It forms the cell membranes in all organs and tissues of the body, is essential to the production of the hormones we need for growth, development, and reproduction, and it makes the bile acids necessary for absorption of nutrients.  Very little, if any, dietary cholesterol becomes serum cholesterol.

Back in the 1990’s it was noted that cholesterol levels below 160 were tied to excess mortality from all causes, primarily from a variety of cancers, respiratory and digestive diseases, and violent deaths from suicide and trauma.  Reasons behind low cholesterol have been ascribed to genetics, resistance to dietary sources, acute infections, and alcohol use/abuse.  (Meilahn.  1995)  If suicide is tied to depression, then it may be a legitimate effect.  Depression is twice as common among women as men, with about one in four suffering at some point in her lifetime.  The greatest vulnerability appears during the childbearing years, the time when its diagnosis is often overlooked.  The turbulence of hormones flooding a woman’s system at different times and in differing amounts can surely be a potent stressor.

Scientists in Barcelona, Spain, realized the connection of cholesterol to neuropsychiatric disease in a review of related literature that preceded their interest.  They found a link to early death, suicide and aggression, and personality disorders and dementia. (Martinez-Carpio.  2009). It appears that the good intentions of reducing what was thought to be the cause of cardiac mortality opened a different can of worms.  The Japanese explored the intrigue that was sparked when total mortality was not reduced despite reduction of mortality due to coronary heart disease, and found an increase in death rates due to suicide and accidents, many of which were tied to risky behaviors in persons with low cholesterol levels.  (Kunugi.  2001)  Does low cholesterol compromise judgment?  The U. of California conducted trials in the early 90’s to determine the cause behind the rise in suicides in men older than fifty years, and found that depression was three times more prevalent in those whose cholesterol was lower than 160.  Health status, number of chronic diseases, number of medications, and exercise seemed not to have had an adverse effect on depressive signs and symptoms. This led to the suggestion that the intentional lowering of cholesterol be more deliberate.  (Morgan. 1993)

Cedars-Sinai Medical Center, in Los Angeles, reported that serotonin, a neurotransmitter that controls impulsive behaviors, is tied to cholesterol levels at the synapses.  Low membrane cholesterol decreases the number of serotonin receptors, thereby reducing suppression of aggressive and destructive behaviors.  (Engelberg. 1992)  That magic number, 160, once again made headlines in the Netherlands, where epidemiologists discovered a higher prevalence of depression in males whose cholesterol was below that level.  (Steegmans. 2000)  Low cholesterol was cited as causative to rises in criminal violence in Sweden, following the association of reduced cholesterol values to low serotonin activity. (Golomb. 2000)  Reduced levels of total cholesterol, LDL, and HDL resulted in minimized serotonin values in personality disordered cocaine users, as reported by addiction researchers in their journal. (Buydens-Branchey. 2000)  In school-aged children, those with cholesterol values lower than 145 were three times more likely to have been suspended or expelled from school.  This is an absolute consideration, and has nothing to do with socio-economic status or ethnic background, nor with nutrition status or academic achievement.  (Zhang. 2005)

Life is supposed to be a balancing act.  Lots of us overdo something.  The balance between total cholesterol and HDL can allay fears of cardiovascular disease, despite cholesterol in the 200 range.  Cholesterol levels below 170 can make us irritable…and irritating.

References

Suarez EC.
Relations of trait depression and anxiety to low lipid and lipoprotein concentrations in healthy young adult women.
Psychosom Med. 1999 May-Jun;61(3):273-9.

Elaine N. Meilahn, MD
Low Serum Cholesterol  Hazardous to Health?
Circulation. 1995;92:2365-2366

Martínez-Carpio PA, Barba J, Bedoya-Del Campillo A.
[Relation between cholesterol levels and neuropsychiatric disorders].  [Article in Spanish]
Rev Neurol. 2009 Mar 1-15;48(5):261-4.

Kunugi H.
[Low serum cholesterol and suicidal behavior].  [Article in Japanese]
Nihon Rinsho. 2001 Aug;59(8):1599-604.

Morgan RE, Palinkas LA, Barrett-Connor EL, Wingard DL.
Plasma cholesterol and depressive symptoms in older men.
Lancet. 1993 Jan 9;341(8837):75-9.

Engelberg H.
Low serum cholesterol and suicide.
Lancet. 1992 Mar 21;339(8795):727-9.

Paul H. A. Steegmans, MD, Arno W. Hoes, MD, PhD, Annette A. A. Bak, MD, PhD, Emiel van der Does, MD, PhD and Diederick E. Grobbee, MD, PhD
Higher Prevalence of Depressive Symptoms in Middle-Aged Men With Low Serum Cholesterol Levels
Psychosomatic Medicine 62:205-211 (2000)

Beatrice A Golomb, Håkan Stattin, Sarnoff Mednick
Low cholesterol and violent crime
Journal of Psychiatric Research. Volume 34, Issue 4 , Pages 301-309, July 2000

Laure Buydens-Branchey, Marc Branchey, Jeffrey Hudson, Paul Fergeson
Low HDL cholesterol, aggression and altered central serotonergic activity
Psychiatry Research. Volume 93, Issue 2 , Pages 93-102, 6 March 2000

Zhang J, Muldoon MF, McKeown RE, Cuffe SP
Association of serum cholesterol and history of school suspension among school-age children and adolescents in the United States.
Am J Epidemiol 2005; 161:691-9.

Scanlon SM, Williams DC, Schloss P.
Membrane cholesterol modulates serotonin transporter activity
Biochemistry. 2001 Sep 4;40(35):10507-13.

Laure Buydens-Branchey,a Marc Branchey,a and Joseph R. Hibbelnb
ASSOCIATIONS BETWEEN INCREASES IN PLASMA N-3 POLYUNSATURATED FATTY ACIDS FOLLOWING SUPPLEMENTATION AND DECREASES IN ANGER AND ANXIETY IN SUBSTANCE ABUSERS
Prog Neuropsychopharmacol Biol Psychiatry. 2008 February 15; 32(2): 568–575.

BRIAN HALLAHAN, MRCPsych and MALCOLM R. GARLAND, MRCPsych
Essential fatty acids and mental health
The British Journal of Psychiatry (2005) 186: 275-277

Hillbrand M, Waite BM, Miller DS, Spitz RT, Lingswiler VM
Serum cholesterol concentrations and mood states in violent psychiatric patients: an experience sampling study.
J Behav Med 2000; 23:519-29.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Essential Fats Explained

fattyacid-sourceThe essential fatty acids (EFA’s) are just that—essential, meaning they have to come from the diet because the body can’t manufacture them. They might be used as fuel, but they are absolute components of the biological processes that make us work. Only two fatty acid families are vital to humans, omega-6’s and omega-3’s. It’s been shown that their ratio is more important than their volume. The parent fatty acid (FA) in the omega-6 (n-6) line is linoleic acid, abundant in many vegetable oils and ultimately responsible for the biosynthesis of arachidonic acid and related prostaglandins, which are compounds that regulate physiological activities. Alpha-linolenic acid (ALA) is the mother omega-3 (n-3) fatty acid, commonly extracted from seed oils such as flaxseed and hemp, but also found in walnuts. Nearly every aspect of human physiology is affected by essential fats, receptors for which are located in practically every cell.

The n-6 fatty acids have been denigrated in recent years because their excess has been linked to several metabolic upsets. Unbalanced diets are harmful to health, and the n-6’s that overpopulate processed foods and rancid supermarket oils have contributed to myriad health woes. What possibly started out as a 1 to 1 or 2 to 1 ratio of n-6 fatty acids to n-3 fatty acids in the human diet eons ago has become a physiological disaster of imbalance, where the ratio exceeds 10 to 1 in the typical Western diet, and may even approach 20 to 1, or worse, in personal food intake. All fatty acids go through a process of desaturation and elongation to become eminently bioactive compounds. The ultimate products of the process are beneficial to human health, especially if they are made step-by-step by the body and not forced upon it through manufactured meals, unnaturally finished meat products, stale/oxidized vegetable oils, and fossilized eggs, not to mention horrific snack foods. In a healthy body, linoleic acid is converted to gamma-linolenic acid (GLA), which becomes arachidonic acid, from which come the chemicals that control inflammation. After adulthood, the body’s ability to make those conversions is uncertain, so starting with GLA gives us a head start. However, mother linoleic acid is anti-inflammatory in its own right and even a marginal conversion to GLA has been held effective in the management of conditions as diverse as rheumatoid arthritis, eczema and ADD/ADHD.

The n-3 parent, ALA, also must come from diet because humans lack the enzymes necessary to convert it from other fats. But it’s the downstream omega-3’s that get the publicity:  EPA and DHA. Like the n-6’s, the conversion of ALA to EPA and later to DHA is an uncertain proposition in adulthood, which is why most adults use fish oil, a source of pre-made fatty acids. Even in the absence of the requisite conversion co-factors (vitamin B6, Mg, biotin, vitamin B3, vitamin C and Zn), ALA is anti-inflammatory and cardiac friendly (Pan, 2012) (Vedtofte, 2012), with recent scrutiny heralding its potential to inhibit progression of atherosclerosis (Bassett, 2011). The most readily available source of ALA is flaxseed, although chia, the newest kid on the block, is entering the marketplace.

Signs of fatty acid deficiency include a dry scaly rash, impoverished growth in youngsters, increased susceptibility to infections and poor wound healing, but are uncommon. The enzymes that convert the parent fatty acids act preferentially toward the n-3’s. By the time these enzymes deal with the omega-3 fats, some of the omega-6’s have been used for energy, hence the need to get more 6’s than 3’s, in a ratio of about 4 to 1, as evidenced by intensive research done in the 1990’s and early-mid 2000’s (Yahuda, 1993, 1996) (Simopoulos, 2002, 2008). But this ratio is based on the body’s own manufacture of the downstream fatty acids, GLA and arachidonic acid (ARA) along the n-6 line (the latter now included in products designed for infants to insure proper brain development) and EPA/DHA down the n-3 line. Deficiency of essential fatty acids sometimes strikes those suffering from cystic fibrosis or fat malabsorption issues. If patients receive total parenteral nutrition without the inclusion of EFA’s, deficit will appear in about a week or two.

The dry weight of the brain is about 80% lipids, the highest of any organ. The long-chain polyunsaturated fats, especially the n-6 and n-3, are crucial in modulating neural function. They occupy as much as 30% of the brain’s dry weight, making their influence on neural membrane dynamics profound. The shift away from EFA’s in the Western—typically American—diet parallels a rise in mental disorders. The need to address EFA supplementation is real and current, with the inclusion of omega-6 fats a necessity, since GLA, the downstream scion of linoleic acid, has held its own in mental health studies (Vaddadi, 2006). Together, the n-6’s and n-3’s cooperate in a number of cellular functions that affect membrane fluidity, allowing the passage of food and energy into the cell and wastes out. Arachidonic acid is a precursor to signaling molecules in the brain and is a key inflammatory intermediate, while EPA and DHA work to support the cardiovascular system, and the brain and retina.

It is arachidonic acid that supports membrane fluidity in the hippocampus, the part of the brain that directs memory, spatial relations and inhibition (Fukaya, 2007). It is arachidonic acid that protects the brain against oxidative stress and activates proteins in charge of the growth and repair of neurons (Darios, 2006). There is conjecture that ARA supplementation during the early stages of Alzheimer’s disease may slow its progress and stave off symptoms (Schaeffer, 2009). That’s a pretty good promise for something that’s been spurned…for lack of knowledge. Of the n-3’s, EPA may be effective in addressing depressive conditions and behavioral anomalies, besides being able to reduce inflammation (Brind, 2001) (Song, 2007). There had been some concern that EPA adversely affects clotting factors and fibrinogen concentrations, increasing the likelihood of bleeding. That is not so (Finnegan, 2003). It does, however, improve blood viscosity and red blood cell deformity, which allows red cells to adjust their shape to squeeze through narrow blood vessels, like capillaries. Downstream from EPA is DHA, a major fatty acid in sperm, brain phospholipids and the retina of the eye, and found to lower triglycerides. But its claim to fame is its rapid accrual in the developing brain during the third trimester of pregnancy and early postnatal period (Auestad, 2003) (Wainwright, 2000).

You can safely bet the farm that endogenous (made by the body itself) substances are more tightly regulated than exogenous. For example, the arachidonic acid your body makes from linoleic acid is more respectable than that from a haphazardly slaughtered steer, which may or may not be completely lifeless before the abattoir starts to dress it. In fear and pain, the animal releases a torrent of adrenal hormones throughout its flesh, confounding the integrity of its innate fatty acids. Endogenous fatty acids are, therefore, more wholesome.

How do we acquire the parent fatty acids?  You could buy oils that boast omega-6 and omega-3 fatty acid content from the supermarket, but it’s almost guaranteed that the balance will be too far out of whack to deliver a benefit, and the purity of the oils is possibly iffy. In fact, they might upset the apple cart. An overabundance of n-3’s can shut the immune system down for lack of guidance by the n-6 inflammation directors. On the other hand, BodyBio Balance Oil is a blend of organic, cold-pressed sunflower and flaxseed oils that are purposely geared to supply a 4 to 1 ratio of fatty acids that the body needs to initiate the cascade to longer chain fats that present vibrant physiological activity. Just the anti-inflammatory properties of the mother fatty acids, linoleic from sunflower and alpha-linolenic from flax, are enough to warrant using the oils to bolster the body’s well-being and to work out some metabolic kinks. Used to make salad dressings or to dress vegetables in place of butter, Balance Oil has the potential to set straight that which is awry, and the essential fatty acid metabolites can help to clear the brain fog on a hazy day. Cerebral lipids, especially the long-chain fatty acids, have significant direct and indirect activity on cerebral function. Not only do they affect the membranes, but also many are converted to neurally active substances. There is good evidence that mental challenges are related to EFA depletion, the supplementation of which can ameliorate the most defiant state of affairs.

References

Auestad N, Scott DT, Janowsky JS, Jacobsen C, Carroll RE, Montalto MB, Halter R, Qiu W, et al
Visual, cognitive, and language assessments at 39 months: a follow-up study of children fed formulas containing long-chain polyunsaturated fatty acids to 1 year of age.
Pediatrics. 2003 Sep;112(3 Pt 1):e177-83.

Bassett CM, McCullough RS, Edel AL, Patenaude A, LaVallee RK, Pierce GN.
The α-linolenic acid content of flaxseed can prevent the atherogenic effects of dietary trans fat.
Am J Physiol Heart Circ Physiol. 2011 Dec;301(6):H2220-6. doi: 10.1152/ajpheart.00958.2010. Epub 2011 Sep 30.

Caramia G.
The essential fatty acids omega-6 and omega-3: from their discovery to their use in therapy.
Minerva Pediatr. 2008 Apr;60(2):219-33.

Chang CS, Sun HL, Lii CK, Chen HW, Chen PY, Liu KL.
Gamma-Linolenic Acid Inhibits Inflammatory Responses by Regulating NF-kappaB and AP-1 Activation in Lipopolysaccharide-Induced RAW 264.7 Macrophages.
Inflammation. 2009 Oct 20.

Darios F, Davletov B.
Omega-3 and omega-6 fatty acids stimulate cell membrane expansion by acting on syntaxin 3.
Nature. 2006 Apr 6;440(7085):813-7.

da Rocha CM, Kac G.
High dietary ratio of omega-6 to omega-3 polyunsaturated acids during pregnancy and prevalence of post-partum depression.
Matern Child Nutr. 2012 Jan;8(1):36-48. doi: 10.1111/j.1740-8709.2010.00256.x. Epub 2010 Jun 21.

Dupasquier CM, Dibrov E, Kneesh AL, Cheung PK, Lee KG, Alexander HK, Yeganeh BK, Moghadasian MH, Pierce GN.
Dietary flaxseed inhibits atherosclerosis in the LDL receptor-deficient mouse in part through antiproliferative and anti-inflammatory actions.
Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2394-402. Epub 2007 Jul 6.

Fernandes FS, de Souza AS, do Carmo Md, Boaventura GT.
Maternal intake of flaxseed-based diet (Linum usitatissimum) on hippocampus fatty acid profile: implications for growth, locomotor activity and spatial memory.
Nutrition. 2011 Oct;27(10):1040-7.

Finnegan YE, Howarth D, Minihane AM, Kew S, Miller GJ, Calder PC, Williams CM.
Plant and marine derived (n-3) polyunsaturated fatty acids do not affect blood coagulation and fibrinolytic factors in moderately hyperlipidemic humans.
J Nutr. 2003 Jul;133(7):2210-3.

Fukaya T, Gondaira T, Kashiyae Y, Kotani S, Ishikura Y, Fujikawa S, Kiso Y, Sakakibara M.
Arachidonic acid preserves hippocampal neuron membrane fluidity in senescent rats.
Neurobiol Aging. 2007 Aug;28(8):1179-86. Epub 2006 Jun 21.

C. Gómez Candela, L. M.ª Bermejo López and V. Loria Kohen
Importance of a balanced omega 6/omega 3 ratio for the maintenance of health.Nutritional recommendations
Nutr Hosp. 2011;26(2):323-329.

Ángeles Guinda, M. Carmen Dobarganes, M. Victoria Ruiz-Mendez, Manuel Mancha
Chemical and physical properties of a sunflower oil with high levels of oleic and palmitic acids
European Journal of Lipid Science and Technology. 105(3-4); Apr 2003: 130-137

BRIAN HALLAHAN, MRCPsych and MALCOLM R. GARLAND, MRCPsych
Essential fatty acids and mental health
The British Journal of Psychiatry (2005); 186: 275-277

William S. Harris, PhD, FAHA, Chair;  Dariush Mozaffarian, MD, DrPH, FAHA;  et al
Omega-6 Fatty Acids and Risk for Cardiovascular Disease
A Science Advisory From the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention
Circulation. 2009; 119: 902-907

Kakutani S, Ishikura Y, Tateishi N, Horikawa C, Tokuda H, Kontani M, Kawashima H, Sakakibara Y, Kiso Y, Shibata H, Morita I.
Supplementation of arachidonic acid-enriched oil increases arachidonic acid contents in plasma phospholipids, but does not increase their metabolites and clinical parameters in Japanese healthy elderly individuals: a randomized controlled study.
Lipids Health Dis. 2011 Dec 22;10:241.

Lands B.
Consequences of essential Fatty acids.
Nutrients. 2012 Sep;4(9):1338-57.

Eric L. LIEN, Kurt STEINER and John C. WALLINGFORD
The Proper Balance of Essential Fatty Acids for Life
Journal of Oleo Science. Vol. 50 (2001) , No. 5 399-405

Maekawa M, Takashima N, Matsumata M, Ikegami S, Kontani M, Hara Y, Kawashima H, Owada Y, Kiso Y, Yoshikawa T, Inokuchi K, Osumi N.
Arachidonic acid drives postnatal neurogenesis and elicits a beneficial effect on prepulse inhibition, a biological trait of psychiatric illnesses.
PLoS One. 2009;4(4):e5085. doi: 10.1371/journal.pone.0005085. Epub 2009 Apr 8.

Osumi N.
Fatty acid signal, neurogenesis, and psychiatric disorders
Nihon Shinkei Seishin Yakurigaku Zasshi. 2010 Jun;30(3):141-8.

Pan A, Chen M, Chowdhury R, Wu JH, Sun Q, Campos H, Mozaffarian D, Hu FB.
α-Linolenic acid and risk of cardiovascular disease: a systematic review and meta-analysis.
Am J Clin Nutr. 2012 Dec;96(6):1262-73. doi: 10.3945/ajcn.112.044040. Epub 2012 Oct 17.

Pawels EK, Volterrani D.
Fatty acid facts, Part I. Essential fatty acids as treatment for depression, or food for mood?
Drug News Perspect. 2008 Oct;21(8):446-51. doi: 10.1358/dnp.2008.21.8.1272136.

Peet M, Brind J, Ramchand CN, Shah S, Vankar GK.
Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment of schizophrenia.
Schizophr Res. 2001 Apr 30;49(3):243-51.

Sakayori N, Maekawa M, Numayama-Tsuruta K, Katura T, Moriya T, Osumi N.
Distinctive effects of arachidonic acid and docosahexaenoic acid on neural stem /progenitor cells.
Genes Cells. 2011 Jul;16(7):778-90. doi: 10.1111/j.1365-2443.2011.01527.x. Epub 2011 Jun 13.

Sanders TA, Rana SK.
Comparison of the metabolism of linoleic and linolenic acids in the fetal rat.
Ann Nutr Metab. 1987;31(6):349-53.

Schaeffer EL, Forlenza OV, Gattaz WF.
Phospholipase A2 activation as a therapeutic approach for cognitive enhancement in early-stage Alzheimer disease.
Psychopharmacology (Berl). 2009 Jan;202(1-3):37-51.

Simopoulos AP.
The importance of the ratio of omega-6/omega-3 essential fatty acids.
Biomed Pharmacother. 2002 Oct;56(8):365-79.

Artemis P. Simopoulos
The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cardiovascular Disease and Other Chronic Diseases
Experimental Biology and Medicine  233:674-688 (2008)

Meharban Singh
Essential fatty acids, DHA and human brain
Indian Journal of Pediatrics. Volume 72, Number 3 / March, 2005: 239-242

Song C, Zhao S.
Omega-3 fatty acid eicosapentaenoic acid. A new treatment for psychiatric and neurodegenerative diseases: a review of clinical investigations.
Expert Opin Investig Drugs. 2007 Oct;16(10):1627-38.

Uauy R, Hoffman DR, Peirano P, Birch DG, Birch EE.
Essential fatty acids in visual and brain development.
Lipids. 2001 Sep;36(9):885-95.

Vaddadi K.
Essential fatty acids and mental illness.
Int Rev Psychiatry. 2006 Apr;18(2):81-4.

Vedtofte MS, Jakobsen MU, Lauritzen L, Heitmann BL
The role of essential fatty acids in the control of coronary heart disease.
Curr Opin Clin Nutr Metab Care. 2012 Nov;15(6):592-6.

Wainwright P.
Nutrition and behaviour: the role of n-3 fatty acids in cognitive function.
Br J Nutr. 2000 Apr;83(4):337-9.

Yehuda S, Carasso RL.
Modulation of learning, pain thresholds, and thermoregulation in the rat by preparations of free purified alpha-linolenic and linoleic acids: determination of the optimal omega 3-to-omega 6 ratio.
Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):10345-9.

Yehuda S, Brandys Y, Blumenfeld A, Mostofsky DI.
Essential fatty acid preparation reduces cholesterol and fatty acids in rat cortex.
Int J Neurosci. 1996 Sep;86(3-4):249-56.

Yehuda S, Rabinovtz S, Carasso RL, Mostofsky DI.
Essential fatty acids preparation (SR-3) improves Alzheimer’s patients quality of life.
Int J Neurosci. 1996 Nov;87(3-4):141-9.

Yehuda S, Rabinovitz S, Mostofsky DI.
Essential fatty acids are mediators of brain biochemistry and cognitive functions
J Neurosci Res. 1999 Jun 15;56(6):565-70.

Yehuda S, Rabinovitz S, Carasso RL, Mostofsky DI.
The role of polyunsaturated fatty acids in restoring the aging neuronal membrane.
Neurobiol Aging. 2002 Sep-Oct;23(5):843-53.

Young G, Conquer J.
Omega-3 fatty acids and neuropsychiatric disorders.
Reprod Nutr Dev. 2005 Jan-Feb;45(1):1-28.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Statins And Diabetes: Why Didn’t They Tell Me?

heart-measureCan you tell when you’ve eaten too much ice cream? Does the eructation shake your table lamps after too many sodas? Sometimes we learn what enough is by having too much. Too bad it isn’t the same with drugs. A hundred-pound lady doesn’t need as many aspirins to get rid of a headache as a two-hundred-pound guy. And for those who take a statin because the doctor said so, why does everybody start with the same doses? With Zocor, everybody starts with 40 mg. Doesn’t anybody think that maybe 5 mg could do the trick? Hey, if one quart of white semi-gloss will cover the bathroom walls adequately, why buy a gallon unless you have a use for it elsewhere? You gonna paint those walls until the gallon is empty?

Over the last few years, the cholesterol model of cardiovascular disease is steadily being replaced by the inflammation model of CVD, putting statin drugs on the back burner because cholesterol, it is realized, has never caused a heart attack. In fact, half the scary cardiac events happen to people who have what are deemed ideal cholesterol numbers (Sachdeva, 2009). Yes, it is true that statins interfere with cholesterol manufacture by the body, not only in the liver, but also in the brain, where cholesterol is vital to the machinery of thought and function. Low cholesterol can lead to serious health issues when that machinery is interrupted.  Low cholesterol levels are associated with high total mortality, even in patients with coronary heart disease (Behar, 1997) (Krumholz, 1994).

Differences between young and old, and between male and female, are recognized in the cholesterol arena, too. The impact of total cholesterol as a risk factor for heart disease decreases with age (Waverling-Rijnsburger, 1997) and for women, whose moderately elevated cholesterol may actually be beneficial (Petursson, 2012). The age cutoff for both genders is fifty (Anderson, 1987). If this information regarding age was known ten years ago, why are TV ads so adamant about getting cholesterol values below a hundred?

The personal experiences of at least one NASA astronaut have attested to the nasty effects of statins, including transient global amnesia, impaired cognition, personality changes, myopathy, neuropathy and neuromuscular degeneration. The root of all these maladies is the inhibition of Co-enzyme Q 10, a physiologically necessary substance that is blocked by Lipitor, Zocor, Crestor and the rest of the gang. Without CoQ10, mitochondria don’t work their magic at cell metabolism, where they get to burn food for energy, oxidize fatty acids, and use the electrons supplied by CoQ10 for a host of other essential activities. The pathway that makes cholesterol also makes CoQ10 in the body. Stopping one stops the other. This is so well known that statin prescriptions in Canada—for Mevachor®, Pravachol® and Lipitor®— contain a warning about CoQ 10 depletion. Merck even filed two patents for a statin-CoQ 10 combination, no. 4,933,165 and no. 4,929,437, which expired in May and June of 2007 (Koon, 2013). And you thought the drug companies had your best interest at heart, eh? The cholesterol issue is a complicated one and now, to add to the quagmire of hits and misses, is the notice that statins are implicated in the risk of developing diabetes. The endearing stars in this drama are atorvastatin (Lipitor), rosuvastatin (Crestor) and simvastatin (Zocor), brought to you by Pfizer, AstraZeneca and Merck. Atorvastatin was found to be the most influential of the three at elevating blood glucose, followed by rosuvastatin and simvastatin, in a recent Canadian study carried out at the Toronto General Hospital (Carter, 2013). From this work it may be drawn that pravastatin (Pravachol) is the safest drug related to diabetes onset. Regardless of drug of choice, or rather the physician’s choice, dose intensity also seems to make a difference in diabetes risk. Intense doses, especially at 80 mg of Zocor, increase the odds of all statin-induced adverse events (Silva, 2007), extending diabetes risk to almost ten percent of the medicated population (Preiss, 2011).

For all the hoopla that accompanied statins’ debut forty years ago into the pharmaceutical world, recounting their anti-cholesterol beneficence, it’s been discovered that their real claim to fame is being anti-inflammatory. That characteristic, it’s claimed, is more important to their raison d’etre than disrupting the cholesterol (and CoQ 10) pathway (Antonopoulos, 2012) (Mora, 2006) (Weitz-Schmidt, 2002). If so, then anti-inflammatory substances that have zero side effects might be considered. In this list will be simple things with complex mechanisms, like ginger, curcumin (from turmeric), capsaicin (from hot peppers), garlic, fish oil, bromelain (from pineapples), flaxseed oil, and zinc, among others. Aside from an allergic reaction which you already would know about, the only side effects of these ingredients are possibly foul breath (that would be the anti-vampire action) and stomach upset from too much of a good thing.

The mention of CoQ10 needs at least a little thought. Natural stores of this enzyme diminish with age. The fact that it donates electrons to multiple body processes bespeaks its importance to full function. It’s comparable to using the correct gauge extension cord with an electric weed trimmer. If the cord can’t carry the voltage, the trimmer will not work to its potential. Adding CoQ 10 to the daily regimen is a prudent decision whether taking a statin or not. Why?  It helps to control blood glucose (Kolahdouz, 2013) (Mezawa, 2012).

References

Anderson KM, Castelli WP, Levy D.
Cholesterol and mortality. 30 years of follow-up from the Framingham study.
JAMA. 1987 Apr 24;257(16):2176-80.

Antonopoulos AS, Margaritis M, Lee R, Channon K, Antoniades C.
Statins as anti-inflammatory agents in atherogenesis: molecular mechanisms and lessons from the recent clinical trials.
Curr Pharm Des. 2012;18(11):1519-30.

Behar S, Graff E, Reicher-Reiss H, Boyko V, Benderly M, Shotan A, Brunner D.
Low total cholesterol is associated with high total mortality in patients with coronary heart disease. The Bezafibrate Infarction Prevention (BIP) Study Group.
Eur Heart J. 1997 Jan;18(1):52-9.

Carter AA, Gomes T, Camacho X, Juurlink DN, Shah BR, Mamdani MM.
Risk of incident diabetes among patients treated with statins: population based study.
BMJ. 2013 May 23;346:f2610. doi: 10.1136/bmj.f2610.

Richard Deichmann, MD, Carl Lavie, MD, and Samuel Andrews, MD
Coenzyme Q10 and Statin-Induced Mitochondrial Dysfunction
Ochsner J. 2010 Spring; 10(1): 16–21.

Forette B, Tortrat D, Wolmark Y.
Cholesterol as risk factor for mortality in elderly women.
Lancet. 1989 Apr 22;1(8643):868-70.

Halfdan Petursson MD, Johann A. Sigurdsson MD Dr med, Calle Bengtsson MD Dr med,
Tom I. L. Nilsen Dr Philos and Linn Getz MD PhD
Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study
Journal of Evaluation in Clinical Practice 18 (2012) 159–168

Risto Huupponen, Jorma Viikari
Statins and the risk of developing diabetes
BMJ. 23 MAY 2013;346:f3156

Kolahdouz Mohammadi R, Hosseinzadeh-Attar MJ, Eshraghian MR, Nakhjavani M, Khorami E, Esteghamati A.
The effect of coenzyme Q10 supplementation on metabolic status of type 2 diabetic patients.
Minerva Gastroenterol Dietol. 2013 Jun;59(2):231-6.

Koon, Robin
CoQ 10 Supplementation with Statins
Natural Products Insider. Feb 26, 2013

Kozarevic D, McGee D, Vojvodic N, Gordon T, Racic Z, Zukel W, Dawber T.
Serum cholesterol and mortality: the Yugoslavia Cardiovascular Disease Study.
Am J Epidemiol. 1981 Jul;114(1):21-8.

Krumholz HM, Seeman TE, Merrill SS, Mendes de Leon CF, Vaccarino V, Silverman DI, Tsukahara R, Ostfeld AM, Berkman LF.
Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years.
JAMA. 1994 Nov 2;272(17):1335-40.

Mezawa M, Takemoto M, Onishi S, Ishibashi R, Ishikawa T, Yamaga M, Fujimoto M, Okabe E, He P, Kobayashi K, Yokote K.
The reduced form of coenzyme Q10 improves glycemic control in patients with type 2 diabetes: an open label pilot study.
Biofactors. 2012 Nov-Dec;38(6):416-21.

Mora S, Ridker PM.
Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER)–can C-reactive protein be used to target statin therapy in primary prevention?
Am J Cardiol. 2006 Jan 16;97(2A):33A-41A.

Steven E. Nissen, M.D., E. Murat Tuzcu, M.D., Paul Schoenhagen, M.D., Tim Crowe, B.S., et al
Statin Therapy, LDL Cholesterol, C-Reactive Protein, and Coronary Artery Disease
N Engl J Med. January 6, 2005; 352:29-38

Preiss D, Seshasai SR, Welsh P, Murphy SA, Ho JE, Waters DD, DeMicco DA, Barter P, et al
Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a meta-analysis.
JAMA. 2011 Jun 22;305(24):2556-64.

Paul M Ridker, M.D., Christopher P. Cannon, M.D., David Morrow, M.D., Nader Rifai, Ph.D, et al
C-Reactive Protein Levels and Outcomes after Statin Therapy
N Engl J Med. Jan 6, 2005; 352:20-28

Rudman D, Mattson DE, Nagraj HS, Caindec N, Rudman IW, Jackson DL.
Antecedents of death in the men of a Veterans Administration nursing home.
J Am Geriatr Soc. 1987 Jun;35(6):496-502.

Sachdeva A, Cannon CP, Deedwania PC, Labresh KA, Smith SC Jr, Dai D, Hernandez A, Fonarow GC.
Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines.
Am Heart J. 2009 Jan;157(1):111-117.e2.

Sattar N, Preiss D, Murray HM, Welsh P, Buckley BM, de Craen AJ, Seshasai SR et al
Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials.
Lancet. 2010 Feb 27;375(9716):735-42.

Sattar N, Taskinen MR.
Statins are diabetogenic–myth or reality?
Atheroscler Suppl. 2012 Aug;13(1):1-10.

Shah RV, Goldfine AB.
Statins and risk of new-onset diabetes mellitus.
Circulation. 2012 Oct 30;126(18):e282-4. doi: 10.1161/CIRCULATIONAHA.112.122135.

Silva M, Matthews ML, Jarvis C, Nolan NM, Belliveau P, Malloy M, Gandhi P.
Meta-analysis of drug-induced adverse events associated with intensive-dose statin therapy.
Clin Ther. 2007 Feb;29(2):253-60.

Simsek S, Schalkwijk CG, Wolffenbuttel BH.
Effects of rosuvastatin and atorvastatin on glycaemic control in Type 2 diabetes—the CORALL study.
Diabet Med. 2012 May;29(5):628-31.

Sukhija R, Prayaga S, Marashdeh M, Bursac Z, Kakar P, Bansal D, Sachdeva R, Kesan SH, Mehta JL.
Effect of statins on fasting plasma glucose in diabetic and nondiabetic patients.
J Investig Med. 2009 Mar;57(3):495-9.

Gabriele Weitz-Schmidt
Statins as anti-inflammatory agents
Trends in Pharmacological Sciences, 1 Oct 2002; Vol 23, Iss 10: 482-487,

Weverling-Rijnsburger AW, Blauw GJ, Lagaay AM, Knook DL, Meinders AE, Westendorp RG.
Total cholesterol and risk of mortality in the oldest old.
Lancet. 1997 Oct 18;350(9085):1119-23.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.