The Evidence And Politics of Prevention

Here is a link to an abstract of Dr Lands indictment of our medical care system with its focus on treatment instead of prevention:
http://www.ncbi.nlm.nih.gov/pubmed/16387724

The abstract is short and simple:

Ann N Y Acad Sci. 2005 Dec;1055:179-92.
Dietary fat and health: the evidence and the politics of prevention: careful use of dietary fats can improve life and prevent disease.
Lands WE.

Abstract
Every year, more young people start the slow progressive injury that eventually becomes cardiovascular disease and death. It could be prevented with nutrition education, but medical efforts focus more on treatments for older people than on preventing primary causes of disease in young people. Two avoidable risks are prevented by simple dietary interventions: (1) Eat more omega-3 and less omega-6 fats, so tissues have less intense n-6 eicosanoid action, and (2) eat less food per meal to lower vascular postprandial oxidant stress. An empirical diet-tissue relationship was developed and put into an interactive personalized software program to aid informed food choices.

He wrote another article that includes the insurance companies. Here is the abstract of that one:
Nutr Health. 2009;20(2):79-89.
False profits and silent partners in health care.
Lands B.

Abstract
Traditional health care services have focused more on treatment of signs and symptoms of cardiovascular disease rather than on prevention of primary causal factors. This bias created a nation with increasing numbers of older people paying for increasing treatment costs. Treatment-oriented clinicians, drug companies and hospitals take a major proportion of ever-increasing health care dollars. Without prevention, American families gain little long-term relief from the highest health care treatment costs in the world. A lack of public accountability for valid surrogate endpoints continues to drain funds for treatments that do not remove underlying primary causes. It seems unethical and uneconomical to withhold community-wide primary prevention advice and only attend to people with clinical signs of disease. Also, treatments that remove a sign or symptom without removing the primary cause unethically set a sense of improved health while leaving unchanged the cause to continue harming future generations. A good alternative would be long-term primary prevention that removes primary causal factors and prevents the onset of signs and symptoms of disease. Health insurance companies could be effective partners with corporate and individual subscribers by diverting resources toward preventing proved primary causes of disease. A chain of molecular events that causally connects modifiable food choices to many health disorders has a measurable mediator: the proportions of omega-3 and omega-6 in tissue highly unsaturated fatty acids (HUFA). Health risk assessment can monitor the diet-based proportions of tissue HUFA which influence hundreds of vital physiologic events. Many financial losses will likely be decreased by primary prevention advice to choose foods that increase intakes of omega-3 fats, decrease intakes of omega-6 fats and include fewer calories per meal.

As I have said before, YOU are the only one with pure interest and benefit from preventing medical problems. Most people do not know about the harm they are doing to their bodies consuming high omega-6 foods. We have heard much more information about the benefits of omega-3, but our food industry simply uses that to make you think a food is healthy when they tell you “It has Omega-3”–they don’t tell you is still has 10 times as much omega-6 and that at that ratio you are still doing harm to your body. Most dietitians are trained in the UDSA guidelines, and they promote many foods that are much higher in omega-6 than omega-3 as healthy–like peanuts and peanut butter.

Look at who benefits from you not knowing this information:
Doctors–they are paid to fix problems not prevent them.
Insurance Companies–they get to keep 20% of health insurance premiums, higher premiums the more that make.
Industrial Agriculture–they grow soybeans, corn, wheat–primary sources of omega-6, they want us eating more.
Food Industry–they love advertising food as healthy without having to pay the cost of healthy food.
Drug companies–they want you to keep taking the pills that treat the problems caused by excess omega-6.

If you are reading this or already know about the harm that comes from excess omega-6, you are one of the lucky ones. The real data is clear–there is an obvious correlation between increasing proportions of omega-6 and many different diseases. Correlation studies are simple and easy to understand, but correlation doesn’t prove cause. The proof comes in the biochemistry that shows the steps in the body’s processing of the lipids and the cellular actions that result from the eicosanoid hormones that are produced from omega-6 and omega-3 lipids. That is far more difficult to understand for most people unless they have an advanced education that includes biochemistry. I do and I can tell you the link between omega-6 and the

    cause

of many diseases is clear.

http://www.amazon.com/dp/B00L5UTY9W#

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Video on balancing omega-6/3

Here is a link to a video by Dr Bill Lands on the benefits of balancing your omega-6/3 ratio.

http://www.efaeducation.org/wellness-videos-balanceimpacts.html

My book teaches you how to reduce omega-6 and increase your omega-3 to achieve a balance. It has list of the amount of omega-6 and omega-3 in a wide variety of foods, recipes with the % omega-6 they will generate and a month of menus.

Available on Amazon for $2.99 (for a limited time)
http://www.amazon.com/dp/B00L5UTY9W

Print version available at Lulu.com for $10.49
http://www.lulu.com/shop/emile-m-lores-jr-phd/the-oil-change-diet/paperback/product-21755800.html

Omega-6 Makes You Fat!

When I started following The Oil-Change Diet, I did it for health reasons, not really expecting it to help me lose weight. I was definitely pleased when I lost 15 pounds in the first 3 weeks, but I knew that weight loss was mostly water weight (from reduced inflammation, swelling and vaso-constriction). I have been really pleased to see the continued weight loss at the rate of a couple pounds per month that has followed and helped me lose what is now a total of 50 pounds.

I have been guessing that the reason was somehow the change in omega-6/3 ratio had changed my serotonin or serotonin receptors, but I finally found a scientific basis for that weight loss: http://www.ncbi.nlm.nih.gov/pubmed/24081493

The paper points out that increased levels of omega-6 in our diet causes an increase in endocannabanoids. As a result, these endocannabanods act like marijuana and give us the munchies. They found that a high percentage of omega-6 whether in a high fat or low fat diet increases these endocannabanoids. Their paper shows that even with a low fat diet, when the ratio of omega-6/3 is high, the omega-6 causes increased adipose tissue (fat).

Here is the abstract:

Dietary linoleic acid elevates the endocannabinoids 2-AG and anandamide and promotes weight gain in mice fed a low fat diet.

Alvheim AR1, Torstensen BE, Lin YH, Lillefosse HH, Lock EJ, Madsen L, Frøyland L, Hibbeln JR, Malde MK.

Author information

Abstract

Dietary intake of linoleic acid (LNA, 18:2n-6) has increased dramatically during the 20th century and is associated with greater prevalence of obesity. The endocannabinoid system is involved in regulation of energy balance and a sustained hyperactivity of the endocannabinoid system may contribute to obesity. Arachidonic acid (ARA, 20:4n-6) is the precursor for 2-AG and anandamide (AEA), and we sought to determine if low fat diets (LFD) could be made obesogenic by increasing the endocannabinoid precursor pool of ARA, causing excessive endocannabinoid signaling leading to weight gain and a metabolic profile associated with obesity. Mice (C57BL/6j, 6 weeks of age) were fed 1 en% LNA and 8 en% LNA in low fat (12.5 en%) and medium fat diets (MFD, 35 en%) for 16 weeks. We found that increasing dietary LNA from 1 to 8 en% in LFD and MFD significantly increased ARA in phospholipids (ARA-PL), elevated 2-AG and AEA in liver, elevated plasma leptin, and resulted in larger adipocytes and more macrophage infiltration in adipose tissue. In LFD, dietary LNA of 8 en% increased feed efficiency and caused greater weight gain than in an isocaloric reduction to 1 en% LNA. Increasing dietary LNA from 1 to 8 en% elevates liver endocannabinoid levels and increases the risk of developing obesity. Thus a high dietary content of LNA (8 en%) increases the adipogenic properties of a low fat diet.

My book, http://www.amazon.com/dp/B00L5UTY9W teaches you how to reduce your omega-6 and lose weight as well as prevent many of the medical problems we face in the US.

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Just because you are young and healthy doesn’t mean omega-6/3 ratio doesn’t matter.

Many people do not pay much attention to their diet as long as they do not perceive themselves as having a diet related problem. However, if you are consuming a typical “Western” or even Mediterranean diet, no matter what your age, you are doing harm to your body because of the excess omega-6.

In a review on efforts to prevent cardiovascular disease by Dr Bill Lands in 2003, he pointed out a study of young soldiers killed in Korea (1953) found that 20% of 15 to 19 yr olds and 40% of 30-34 yr olds already had signs of fatty deposits in their descending aortas. He also points out that clinicians and the health community in general wait until disease symptoms appear before designing treatments instead of providing preventive education much earlier.

In many individuals, the first sign or coronary artery disease is sudden death, but the cause of the disease is long-term chronic inflammatory process involving excessive omega-6 autacoids (hormones made from omega-6 lipids). Preventing heart disease and many other diseases related to excessive omega-6 intake requires educating individuals about the dietary sources of omega-6 and consequences of excessive omega-6 well before symptoms appear.

The simple process of educating individuals about omega-6 is difficult. There is too much conflicting information coming from sources of dietary information. Most dietitians get their information from USDA dietary guidelines–USDA works for farmers. Dietitians often have little or no understanding of the bio-chemical causes of disease. Even many doctors do not know or understand the biochemical processes behind many of the diseases they treat. Doctors don’t really have a monetary interest in preventing disease and often spend little time dealing with healthy patients before problems appear.

Dr Lands and a few other doctors are trying to educate people about the consequences of excessive omega-6 and the dietary information needed to avoid it. I was fortunate to find the information on omega-6 when I did, I can only wish I had found this information sooner.

Omega-3, 6/3 Ratio and Pain

Below is part of a publication by Dr Gordon on the effect of omega-3 on pain and inflammation. One of the studies he points to found 59% of arthritic patients were able to discontinue use of NSAIDS and substitute Omega-3 supplements for control of their arthritic pain. I am certainly one that would be in the 59% group. The pain relief does not just apply to arthritic patients. The bottom line–if you have pain– follow The Oil-Change Diet.

Omega-3 Fatty Acids and Neuropathic Pain
Case studies demonstrate that oral intake of omega-3
polyunsaturated fatty acids from pharmaceutical-grade fish oil
supplements results in pain reduction and functional improvement
in patients with neuropathic pain.
By Gordon D. Ko, MD, CCFP(EM), FRCPC, PhD, Leigh Arseneau, BSc, ND, Nathaniel Nowacki, BA and Serge Mrkoboda, BSc

PUFAs and Eicosanoid Metabolism
The n-3 and n-6 fatty acids are chemically and metabolically distinct and have contrasting physiological functions12 (see Figure 4). The eicosanoid metabolic products synthesized from AA, namely prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), hydroxy fatty acids and lipoxins are formed in larger quantities than those formed from n-3 PUFAs—such as EPA—because of the increased amounts of n-6 PUFAs in the Western diet.1 Eicosanoids derived from AA are biologically active in small quantities and, if they are formed in inordinate amounts, they contribute to the formation of atheromas and thrombi.1 In addition, they lead to the development of allergic and inflammatory disorders and to cell proliferation.

When humans increase their consumption of EPA and DHA, from oily fish or from fish oil supplements (liquids or capsules), an increased proportion of these fatty acids are found in the cell membranes of inflammatory cells in particular.14 EPA and DHA incorporation into these membranes occurs in a dose-response fashion and is partly at the expense of AA.15 Hence, since there is less AA available for eicosanoid biosynthesis by the cyclooxygenase (COX) and lipoxygenase (LOX) enzymes, fish oil supplementation of the diet results in a decreased production of the proinflammatory prostaglandin E2 (PGE2), thromboxane A2 (TXA2), TXB2, leukotriene B4 (LTB4), LTE4 and 5-hydroxyeicosatetraenoic acid, but not of prostacyclin I2 (PGI2).12,14

EPA can also act as a substrate for both COX and LOX enzymes and thereby compete with AA for prostaglandin and leukotriene synthesis.12 EPA gives rise to the 3-series PGs and TXs (such as TXA3, PGE3, PGI3) and to the 5-series LTs (LTB5, LTE5) and 5-hydroxyeicosapentaenoic acid.14 The eicosanoids formed from EPA are frequently less biologically potent than those formed from AA.15 For example, LTB5 is 10- to 100- fold less potent as a neutrophil chemotactic agent than LTB4 and PGE3 is a less potent inducer of COX-2 gene expression in fibroblasts than PGE2.15 Furthermore, TXA3 is a weaker platelet aggregator and vasoconstrictor than TXA2.12 Recent studies have shown that EPA and DHA also give rise to resolvins (from EPA and DHA) and docosanoids (from DHA) through pathways involving COX and LOX enzymes.16 In cell culture and animal-feeding studies, these novel mediators were demonstrated to be anti-inflammatory, inflammation resolving, and immu-nomodulatory.16

Some of the effects of n-3 PUFAs are elicited by eicosanoid-independent mechanisms. Studies have shown, for example, that the intake of dietary fish oil results in decreased leukocyte chemotaxis, decreased expression of adhesion molecules and decreased generation of reactive oxygen species.15 n-3 PUFAs have also been shown to inhibit the production of proinflammatory cytokines such as tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), IL-6 and IL-8, in both cell culture studies and in human trials.14,15 Additionally, n-3 PUFAs might exert their effects on inflammatory gene expression through direct action on intracellular signaling pathways which lead to activation of one or more transcription factors such as nuclear factor kappa B (NF-kb).14

Figures 4. Pathways to inflammation: omega-6 is pro-inflammatory and omega-3 is anti-inflammatory.

n-3 PUFAs and Chronic Disease
The benefits of n-3 PUFA supplementation are well documented in the literature for the prevention and management of a wide variety of health conditions including inflammatory and autoimmune diseases, cardiovascular disease, and depression. Less is known, however, about the use and efficacy of these fatty acids in the treatment of other disorders such as fibromyalgia syndrome and neuropathic pain.

n-3 PUFAs and Inflammatory/ Autoimmune Diseases
A number of clinical trials have been conducted assessing the benefits of dietary supplementation with n-3 PUFAs in inflammatory and autoimmune disease in humans, including RA, Crohn’s diseases, ulcerative colitis, psoriasis, lupus erythematosus, MS, and migraine headaches.12

A recent meta-analysis of 17 randomized controlled trials (RCTs) was conducted by Goldberg et al. to assess the pain relieving effects of n-3 PUFAs in patients with rheumatoid arthritis (RA) or joint pain secondary to inflammatory bowel disease and dysmenorrhea.17 Results from the analysis showed that supplementation with n-3 PUFAs for 3-4 months reduces patient-reported joint pain intensity, minutes of morning stiffness, number of painful and/or tender joints, and NSAID consumption.

Maroon et al. conducted a non-placebo controlled study to determine if patients could effectively substitute fish oil as an anti-inflammatory for NSAIDs.18 The study included 250 participants who had been seen by a neurosurgeon and were found to have chronic, nonsurgical, neck or back pain. After taking n-3 PUFAs for an average of 75 days, 59% discontinued their use of prescription NSAIDs and 60% stated that their overall pain was improved. Moreover, 88% stated they would continue to take the n-3 PUFAs. No significant adverse effects were reported. These results corroborate other controlled studies that compared ibuprofen and n-3 PUFAs demonstrating equivalent effects in reducing arthritic pain.18 Furthermore, such findings suggest that n-3 PUFAs may be a safe alternative to NSAIDs, particularly the COX-2 inhibitors which have been associated with extreme complications such as gastric ulcers, bleeding, blood pressure increase, myocardial infarction, and even death.19

In clinical trial, nutrient mixture developed at MIT improves memory in patients with early Alzheimer’s

DHA, the omega-3 lipid, as part of a nutrient cocktail, has been shown to reliably reverse symptoms of Alzheimer’s in clinical trials. This is a first and a promising treatment for this devastating disease, but it also shows the importance of diet in preventing this disease.

ClinicalNews.Org

Nutrient mixture improves memory in patients with early Alzheimer’s

A graphic depicting a synapse, a connection between brain cells. Photo – Graphic: Christine Daniloff

Anne Trafton, MIT News Office

July 9, 2012

A clinical trial of an Alzheimer’s disease treatment developed at MIT has found that the nutrient cocktail can improve memory in patients with early Alzheimer’s. The results confirm and expand the findings of an earlier trial of the nutritional supplement, which is designed to promote new connections between brain cells. Alzheimer’s patients gradually lose those connections, known as synapses, leading to memory loss and other cognitive impairments. The supplement mixture, known as Souvenaid, appears to stimulate growth of new synapses, says Richard Wurtman, the Cecil H. Green Distinguished Professor Emeritus at MIT, who invented the nutrient mixture. “You want to improve the numbers of synapses, not by slowing their degradation — though of course you’d love to do…

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Why doctors aren’t talking about omega-6.

Here is a link to and article by Dr Bill Lands about why doctors are not really treating the cause of heart disease–omega-6: http://www.fastlearner.org/Bill’s%20Papers/2003Review.pdf

Doctors are biased toward using expensive procedures to fix medical problems–that is where a lot of their money comes from. Doctors pay more attention to drug treatments than to dietary remedies. Even if they do pay attention to dietary studies, they want simple studies that compare one diet to another instead of complex biochemical studies that seek to understand the complex cause of diseases.

Insurance companies don’t care either, the higher the cost of medical treatments, the more they can justify higher rates. They get to keep 20% of the cost of their policy holder pay, so the more you pay the more they get to keep.

Only the people ultimately paying for medical cost–you and I–are really interested in reducing medical problems and their associated cost. The problem is that most people do not have the knowledge to understand the biochemical causes of disease. I have the ability to understand the biochemistry and the chemical terminology, but until I began to research the effects of lipids in my diet, I was unaware of the studies that make it clear to me that excess omega-6 is behind many of the medical problems that I was dealing with personally. In my book, I try to make it simple and easy for people that do not have the ability to understand chemistry and biochemistry and just show you what foods you need to avoid and the ones you need to increase in your diet. I also provide the chemistry and biochemistry, which for most people would probably be a good sleeping aid.

My recipes and menu will help you learn how to prepare truly healthy meals and my list of lipid content of various foods will help you select the kinds of foods that are lower in omega-6 and higher in omega-3.

http://www.lulu.com/shop/emile-m-lores-jr-phd/the-oil-change-diet/paperback/product-21755800.html
http://www.amazon.com/dp/B00L5UTY9W

You don’t need to eat a lot of fish

Here is an abstract from an article that points out that you don’t need to eat a lot of fish (omega-3) to have a healthy balance–you just need to eat a lot less omega-6. My book teaches you how to reduce the omega-6 in your diet. Here is the abstract (an explanation to help you understand it follows the abstract):

Am J Clin Nutr. 2006 Jun;83(6 Suppl):1483S-1493S.
Healthy intakes of n-3 and n-6 fatty acids: estimations considering worldwide diversity.
Hibbeln JR1, Nieminen LR, Blasbalg TL, Riggs JA, Lands WE.
Author information
Abstract
BACKGROUND:
The worldwide diversity of dietary intakes of n-6 and n-3 fatty acids influences tissue compositions of n-3 long-chain fatty acids (LCFAs: eicosapentaenoic, docosapentaenoic, and docosahexaenoic acids) and risks of cardiovascular and mental illnesses.
OBJECTIVE:
We aimed to estimate healthy dietary allowances for n-3 LCFAs that would meet the nutrient requirements of 97-98% of the population.
DESIGN:
Deficiency in n-3 LCFAs was defined as attributable risk from 13 morbidity and mortality outcomes, including all causes, coronary heart disease, stroke, cardiovascular disease, homicide, bipolar disorder, and major and postpartum depressions. Dietary availability of n-3 LCFAs from commodities for 38 countries and tissue composition data were correlated by best fit to each illness in deficiency risk models.
RESULTS:
The potential attributable burden of disease ranged from 20.8% (all-cause mortality in men) to 99.9% (bipolar disorder). n-3 LCFA intake for Japan (0.37% of energy, or 750 mg/d) met criteria for uniformly protecting >98% of the populations worldwide. n-3 LCFA intakes needed to meet a tissue target representative of Japan (60% n-3 in LCFA) ranged from 278 mg/d (Philippines, with intakes of 0.8% of energy as linoleate, 0.08% of energy as alpha-linolenate, and 0.06% of energy as arachidonic acid) to 3667 mg/d (United States, with 8.91% of energy as linoleate, 1.06% of energy as alpha-linolenate, and 0.08% of energy as arachidonic acid).
CONCLUSIONS:
With caveats inherent for ecologic, nutrient disappearance analyses, a healthy dietary allowance for n-3 LCFAs for current US diets was estimated at 3.5 g/d for a 2000-kcal diet. This allowance for n-3 LCFAs can likely be reduced to one-tenth of that amount by consuming fewer n-6 fats.

Explanation: n-3 LCFA is their term for Omega-3 fatty acid. Design: They point out that deficiency in omega-3 has been shown to be related to 13 different causes of death and correlated the availability of omega-3 in 38 different countries to each illness. Results: Omega-3 is related to all causes of death in 20.8% of all cases, but has a 99.9% correlation with bipolar disorder (that is amazing to me). They used the omega-3 intake in Japan as a reference level since it protects 98% of the population. In Japan they only need 750 mg/day of omega-3 (representing 0.37% of their food energy intake) to maintain their level of omega-3 in their tissue level of 60% omega-3. In the Philippines they only need 278 mg/day (because their intake of omega-6 is so low), while in the US, we need 3,667 mg of omega-3/day–because most Americans consume so much omega-6.

The bottom line is that you don’t really have to eat a lot of fish–you just have to avoid the omega-6. This is the missing information in our dietary recommendations. That is what my book is trying to teach people!

http://www.amazon.com/dp/B00L5UTY9W
http://www.lulu.com/shop/emile-m-lores-jr-phd/the-oil-change-diet/paperback/product-21755800.html