Mar
25
2017

How Stress Affects Our Hormone System

Dr. Andrew Heyman gave a talk recently about how stress affects our hormone system. His talk was presented at the 24th Annual World Congress on Anti-Aging Medicine (Dec. 9-11, 2016) in Las Vegas that I attended. It was entitled “Understanding the Stress, Thyroid, Hormone Connections & Prioritizing Systems”.

Dr. Heyman stressed that there is a triad of hormonal connections that is important to remember: the thyroid hormones, the stress hormones (adrenal glands) and the pancreas (insulin production). We need a balance of these hormones for optimal energy production and circulation. Under stress our sugar metabolism can derail, we develop obesity and fatigue. When balanced we experience vitality and wellbeing.

Metabolic activation pathways

Dr. Heyman projected a slide that showed the metabolic activation pathways. He stated that a number of different factors could influence the hormone system:

  • Diet: trans fats, sugar, too many carbs, food allergies.
  • Drugs: drug-induced nutrient depletion (over-the-counter drugs, prescription drugs).
  • Physical exercise: frequency and type matters.
  • Environmental exposure: chemicals, pesticides, herbicides, heavy metals, plastics, molds, and pollens.
  • Stress: physical stress, psychogenic stress.
  • Genetics: methylene-tetra-hydro-folate reductase enzyme deficiency (MTHFR mutation), APOE genes, lack of vitamin D
  • Disease: past or present conditions, active disease or syndromes.

Target areas within your system

The target areas in your system are the

  • Pancreas, where blood sugar can rise because of insulin resistance. Too much insulin production causes inflammation, hormone disbalances, kidney damage, and hardening of the arteries through plaque formation.
  • Thyroid gland, which gets activated by TSH (thyroid stimulating hormone), but can also be affected negatively by autoantibodies).
  • Brain: decrease in serotonin resulting in anxiety, depression and food cravings; decreased melatonin causing sleep disturbances; increased ghrelin and decreased leptin secretion leading to overeating and obesity.
  • Liver/kidneys: both of these organs are important for detoxification; the liver produces thyroid binding globulin, which when increased can lower the free thyroid hormones.
  • Immune system (gut, lymph glands): the Peyer’s patches in the gut mucosa produce a large portion of the immune cells; lymph glands, the bone marrow and the spleen supply the rest. A leaky gut syndrome can affect the whole body, causing inflammation and autoimmune reactions.
  • Hypothalamus/pituitary/adrenal glands: this is the main axis of the stress reaction. If the brain is stressed, the hypothalamus sends a cascade of activating hormones via the pituitary gland and the adrenal glands. This leads to cortisol overproduction, and release of epinephrine and norepinephrine from the center of the adrenal glands. High blood pressure, anxiety, heart palpitations, arrhythmias and more can develop from this.

Hypothalamus/pituitary/adrenal glands activation and clinical effects

The main hormone axis of the stress reaction goes from the hypothalamus via the pituitary gland to the outside surface of the adrenal glands where cortisol is released. It is also called the HPA axis. Stressed people make too much cortisol, which weakens immune functions, reduces human growth hormone production, increases belly fat, increases blood pressure and reduces insulin action. Stress also reduces estrogen production in women and testosterone production in men.

The final clinical presentation is osteopenia, then osteoporosis with spontaneous fractures of bones. There is cardiovascular disease leading to heart attacks and strokes, and cognitive decline with memory loss. There are complications with infections. Also the metabolic syndrome can lead to obesity and type 2-diabetes.

Stress and the hippocampus

In the center of our brain there is a memory-processing unit, the hippocampus that converts short-term memory into long-term memory. Repeated stress interferes with normal hippocampus function. High cortisol levels interfere with the proper functioning of the hippocampus causing memory problems.

Chronically elevated cortisol levels from chronic stress have been shown to lead to hippocampus atrophy and can cause Alzheimer’s disease.

Effects of chronic stress

Chronic stress leads to cardiovascular disease, to diabetes, chronic inflammation, Alzheimer’s disease, thyroid disorders, cancer, neurological disorders and autoimmune diseases. Inflammation research has shown that with chronic inflammation tumor necrosis factor-alpha (TNF-alpha) is released, as key player of chronic inflammation. This however leads to the release of other inflammatory kinins like IL6 and others. The resulting chronic inflammation can cause Crohn’s disease, rheumatoid arthritis, insulin resistance, dementia, metabolic syndrome, obesity and atherosclerosis with associated markers (decreased HDL, increased LDL, CRP and triglycerides).

Hormone imbalance causes disease

  1. Excess cortisol production from stress leads to Th2 type inflammatory kinins; usually associated with this is a reduction of DHEA (a male hormone in the adrenal glands), which leads to reduced Th1 type kinins. The end result is chronic inflammation. When chronic stress has tired out the adrenal glands, a four-point salivary cortisol level test shows a flat curve. This indicates adrenal gland fatigue or, if worse, even adrenal gland insufficiency. Such a pattern is found in patients with leukemia, breast cancer, uterine cancer, prostate cancer, pituitary gland cancer and lung cancer.
  2. The metabolic syndrome is associated with dysregulation of the HPA axis. People who have this syndrome have a high morning serum cortisol level. High cortisol increases the risk to develop metabolic syndrome.
  3. Metabolic connections: high cortisol leads to a partial blockage of thyroid hormones, which in turn leads to hypothyroidism. Hypothyroidism will affect glucose tolerance, and if not treated leads to type 2 diabetes.

In a large study involving 46,578 members of Kaiser Permanente Northwest it was determined that for every 1 point above a fasting glucose level of 84 mg/dL there was an additional 6% risk to develop type 2 diabetes over the next 10 years.

Pathological hormone disturbances

The following hormone patterns were discussed in detail, an increased cortisol level, increased insulin level and decreased thyroid levels.

Elevated cortisol

Prolonged elevation of cortisol leads to atrophy of the hippocampus with brain atrophy and Alzheimer’s or dementia. The immune system gets altered, there is lower DHEA hormone leading to weaker muscles and weakened immunity. There is insulin resistance (decreased insulin sensitivity), decreased serotonin and increased depression. Carbohydrate cravings lead to weight gain (central obesity). Changes in the thyroid metabolism leads to hypothyroidism.

Increased insulin level

People who develop high insulin levels are usually sugar or carbohydrate addicts. As they gain weight they change their metabolism into the metabolic syndrome. The extra insulin that is floating around triggers the insulin receptors to become less sensitive (also called “resistant”). The people love to eat. They snack frequently on protein bars and candy bars. As they gain weight, their energy goes down and they often develop painful joints. This prevents them from being physically active. They notice episodes of foggy thinking. Women complain of frequent yeast infections.

The body tries to compensate by slightly decreasing thyroid hormones and slightly increasing cortisol levels.

Decreased thyroid levels

There is increased lactic acid production and decreased insulin sensitivity. Oxidative stress is increased. The patient is depressed and cognition and memory are reduced. The gut has slower motility. The mitochondria, the energy packages in each cell are reduced and functioning less productively. Cardiac function is reduced.

The body tries to compensate for the primary thyroid weakness by slightly elevating insulin and cortisol.

Treatment of stressed hormone system

Before the doctor can treat a disbalanced hormone system, blood tests have to be done that show what kind of hormone constellation is present. Dr. Heyman suggested the following support with supplements.

Treatment of thyroid disorders

Thyroid supplementation may involve any of these: Selenomethionine, iodine, chromium, thyroid glandular, tyrosine, ferritin, Ashwagandha, coleus forskohlii, 7-keto DHEA, ferritin and iron. Other possible supplements that were mentioned by Dr. Heyman were Rhodiola, schisandra, ginseng, Rg3, eurycoma longifolia, neuromedulla glandular, DHEA, tryptophan/5 HTP, licorice, Cordyceps.

This, however, is not all. Missing thyroid hormones have to be replaced with a balanced T3/T4 medication like Armour thyroid.

Adrenal support

The following supplements are used to support adrenals: Adrenal glandular, vitamin C, adrenal cortex extract, Holy Basil, Pharma GABA, Magnolia/Phellodendron, L-theanine, sterols & sterolins.

Pancreatic support

These supplements support the insulin production in the pancreas:

Chromium, vitamin D, magnesium, alpha-lipoic acid, fish oil, micro PQQ, bitter melon, cinnamon, arginine, vanadium, benfotiamine (synthetic derivative of B1 vitamin) and Bergamot.

Dr. Heyman completed his talk by giving a few patient examples, explaining what blood tests showed, what the hormone disbalance was, and which treatment options were helpful.

How Stress Affects Our Hormone System

How Stress Affects Our Hormone System

Conclusion

Dr. Andrew Heyman gave a talk at the 24th Annual World Congress on Anti-Aging Medicine (Dec. 9-11, 2016) in Las Vegas that I attended. He talked about how stress affects our hormone system. Symptoms from stress can stem from different causes including hormone disbalances. Conventional medicine would simply treat the symptoms. However, this will not be successful with stress-induced hormone disbalances, because it does not treat the causes. Causal treatment of the hormone disbalance will restore the person’s wellbeing and the symptoms will disappear at the same time. Anti-aging medicine and integrative medicine are attempting to follow this approach.

Feb
25
2017

Heart Health Improves With Hormone Replacement

Dr. Pamela Smith gave a lecture in December 2016 showing that heart health improves with hormone replacement. Her talk was part of the 24th Annual World Congress on Anti-Aging Medicine (Dec. 9 to Dec. 11, 2016) in Las Vegas, which I attended. The title of the talk was: “Heart health: The Importance of Hormonal Balance for Men and Women”. Her keynote lecture contained 255 slides. I am only presenting a factual summary of the pertinent points here.

1. Estrogen

Observations regarding risk of heart attacks

  1. Women have a lower risk of heart attacks before menopause compared to men of the same age.
  2. Heart attack rates go up significantly after menopause.
  3. Estrogen replacement therapy may reduce the risk of heart attacks by 50% for postmenopausal women.

Lipid profile after menopause

There is an elevation of LDL cholesterol, total cholesterol and triglycerides as well as lower HDL cholesterol levels. All of this causes a higher risk of heart attacks for postmenopausal women. Estrogen replacement therapy increases the large VLDL particles, decreases LDL levels and raises HDL-2. These changes are thought to be responsible for helping reduce heart attack rates in postmenopausal women who do estrogen replacement therapy (ERT).

Difference between oral and transdermal estrogen replacement

When estrogen is taken by mouth, it is metabolically changed in the liver. This reduces the protective effect on the cardiovascular system. In contrast, transdermal estrogen (from commercial estrogen patches or from bioidentical estrogen creams) has a higher cardioprotective effect. The liver does not metabolize transdermal estrogen. Dr. Smith explained in great detail using many slides how estrogen prevents heart attacks. Details about this would be too technical for this review. Apart from lipid lowering effects there are protective effects to the lining of the arteries. In addition there are metabolic processes in heart cells and mitochondria that benefit from estrogens. The end result is that postmenopausal women who replace estrogen will outlive men by about 10 years. Stay away from Premarin, which is not human estrogen, but is derived from pregnant mares. Also the tablet form is metabolized by the liver, which loses a lot of the beneficial effects that you get from transdermal estrogen. 

How can you document the beneficial effects of estrogen replacement?

  1. Carotid intima measurements in postmenopausal women on ERT show a consistent reduction in thickness compared to controls.
  2. The physical and emotional stress response is reduced compared to postmenopausal women without ERT.
  3. Hormone replacement therapy in postmenopausal women reduces blood pressure. Measurements showed this effect to be due to a reduction of angiotensin converting enzyme (ACE) by 20%. This is the equivalent of treating a woman with an ACE inhibitor without the side effects of these pills.
  4. Coronary calcification scores were lower in postmenopausal women on ERT than a control group without ERT. These calcification scores correlate with the risk for heart attacks.
  5. Oral estrogen replacement leads to proinflammatory metabolites from the liver metabolism of estrogen. This is not found in the blood of women using transdermal estrogen. The anti-inflammatory effect of transdermal estrogen is another mechanism that prevents heart attacks.
  6. Postmenopausal women on ERT had no increased risk of heart attacks or venous thromboembolism (clots in veins). Menopausal women without ERT have a risk of 40% of dying from a heart attack. Their risk of developing breast cancer is 5.5%, the risk of dying from breast cancer is about 1%. Oral estrogen use was associated with venous thromboembolism.
  7. Estrogen has antiarrhythmic effects stabilizing the heart rhythm. Dr. Smith said that in the future intravenous estrogen might be used to prevent serious arrhythmias following heart attacks.

Estrogen levels in males

Males require a small amount of estrogens to maintain their memory, for bone maturation and regulation of bone resorption. But they also need small amounts of estrogen for their normal lipid metabolism.

However, if the estrogen levels are too high as is the case in an obese, elderly man, there is an increased risk of heart disease. Factors that lead to increased estrogen levels in an older man are: increased aromatase activity in fatty tissue, overuse of alcohol and a change in liver metabolism, zinc deficiency, ingestion of estrogen-containing foods and environmental estrogens (also called xenoestrogens).

2. Progesterone

Progesterone is significantly different from the progestin medroxyprogesterone (MPA). MPA was the oral progestin that was responsible for heart attacks and blood clots in the Women’s Health Initiative. MPA increases smooth muscle cell proliferation. This in turn causes hardening of the coronary arteries. In contrast, progesterone inhibits smooth muscle cell proliferation, which prevents heart attacks. Progesterone also lowers blood pressure and elevates HDL cholesterol, but MPA does not.

Progesterone in males

In a small study Depo-Provera was given to males for 17 days. Blood tests showed a lowering of triglycerides, LDL cholesterol and Apo A-1.

3. Testosterone

Testosterone replacement in women

Testosterone in women does not only increase their sex drive, but also relaxes the coronary arteries in women who were testosterone deficient. This allows more blood flow to the heart. In postmenopausal women testosterone replacement lowered lipoprotein (a) levels up to 65%. The physician will only replace testosterone in women who have either enough of their own estrogen production or else have been replaced first with bioidentical estrogen. Otherwise testosterone alone can cause heart attacks in women.

Elevated testosterone in women with PCOS

Women with polycystic ovary syndrome (PCOS) can have increased testosterone levels when they go through premenopause or menopause.

Women with PCOS are at a higher risk to develop diabetes, heart disease and high blood pressure. 50% of women with PCOS have insulin resistance. 70% of women with PCOS in the US have lipid abnormalities in their blood.

Elevated testosterone levels in the blood can lower the protective HDL cholesterol and increase homocysteine levels. Both can cause heart attacks.

Women with PCOS have a 4-fold risk of developing high blood pressure.

Testosterone replacement in males

A 2010 study showed that low testosterone levels in males were predictive of higher mortality due to heart attacks and cancer. Low testosterone is also associated with high blood pressure, heart failure and increased risk of cardiovascular deaths. There was a higher incidence of deaths from heart attacks when testosterone levels were low compared to men with normal testosterone levels.

Low testosterone is also associated with the development of diabetes and metabolic syndrome, which can cause heart attacks.

It is important that men with low testosterone get testosterone replacement therapy.

DHT (Dihydrotestosterone)

DHT is much more potent than testosterone. Conversion of testosterone leads to DHT via the enzyme 5-alpha-reductase. While testosterone can be aromatized into estrogen, DHT cannot. Some men have elevated levels of DHT. This leads to a risk of heart attacks, prostate enlargement and hair loss of the scalp.

Andropause treatment

Only about 5% of men in andropause with low testosterone levels receive testosterone replacement in the US. Part of this is explained by rumors that testosterone may cause prostate cancer or liver cancer. The patient or the physician may be reluctant to treat with testosterone. Bioidentical testosterone has been shown to not cause any harm. It is safe to use testosterone cream transdermally. It does not cause prostate cancer or benign prostatic hypertrophy.

An increase of 6-nmol/L-serum testosterone was associated with a 19% drop in all-cause mortality.

Testosterone helps build up new blood vessels after a heart attack. Testosterone replacement increases coronary blood flow in patients with coronary artery disease. Another effect of testosterone is the decrease of inflammation. Inflammation is an important component of cardiovascular disease.

Testosterone replacement improves exercise capacity, insulin resistance and muscle performance (including the heart muscle).

Apart from the beneficial effect of testosterone on the heart it is also beneficial for the brain. Testosterone treatment prevents Alzheimer’s disease in older men by preventing beta amyloid precursor protein production.

4. DHEA

Dehydroepiandrosterone (DHEA) is a hormone produced in the adrenal glands. It is a precursor for male and female sex hormones, but has actions on its own. It supports muscle strength. Postmenopausal women had a higher mortality from heart disease when their DHEA blood levels were low.

Similar studies in men showed the same results. Congestive heart failure patients of both sexes had more severe disease the lower the DHEA levels were. Other studies have used DHEA supplementation in heart patients, congestive heart failure patients and patients with diabetes to show that clinical symptoms improved.

5. Melatonin

Low levels of melatonin have been demonstrated in patients with heart disease. Melatonin inhibits platelet aggregation and suppresses nighttime sympathetic activity (epinephrine and norepinephrine). Sympathetic activity damages the lining of coronary arteries. Melatonin reduces hypoxia in patients with ischemic stroke or ischemic heart disease. Lower nocturnal melatonin levels are associated with higher adverse effects following a heart attack. Among these are recurrent heart attacks, congestive heart failure or death. Melatonin widens blood vessels, is a free radical scavenger and inhibits oxidation of LDL cholesterol. Melatonin reduces inflammation following a heart attack. This can be measured using the C-reactive protein.

In patients who had angioplasties done for blocked coronary arteries intravenous melatonin decreased CRP, reduced tissue damage, decreased various irregular heart beat patterns and allowed damaged heart tissue to recover.

6. Thyroid hormones

It has been known for more than 100 years that dysfunction of the thyroid leads to heart disease. Hypothyroidism can cause heart attacks, hardening of the coronary arteries and congestive heart failure. Lesser-known connections to hypothyroidism are congestive heart failure, depression, fibromyalgia, ankylosing spondylitis and insulin resistance. Some cases of attention deficit hyperactivity disorder (ADHD) with low thyroid levels may successfully respond to thyroid replacement.

Thyroid hormones improve lipids in the blood, improve arterial stiffness and improve cardiac remodeling following a heart attack. Thyroid hormones help with the repair of the injured heart muscle. They also work directly on the heart muscle helping it to contract more efficiently. Lower thyroid stimulating hormone (TSH) values and higher T3 and T4 thyroid hormone levels lead to improved insulin sensitivity, higher HDL values (= protective cholesterol) and overall better functioning of the lining of the arteries.

Dr. Smith said that thyroid replacement should achieve that

  • TSH is below 2.0, but above the lower limit of normal
  • Free T3 should be dead center of normal or slightly above
  • Free T4 should be dead center of normal or slightly above

Most patients with hypothyroidism require replacement of both T3 and T4 (like with the use of Armour thyroid pills).

7. Cortisol

Cortisol is the only human hormone that increases with age. All other hormones drop off to lower values with age. The adrenal glands manufacture cortisol. With stress cortisol is rising, but when stress is over, it is supposed to come down to normal levels. Many people today are constantly overstressed, so their adrenal glands are often chronically over stimulated. This can lead to a lack of progesterone. It also causes a lack of functional thyroid hormones as they get bound and are less active. When women have decreased estradiol in menopause there is a decline in norepinephrine production, production of serotonin, dopamine and acetylcholine. Women with this experience depression, lack of drive and slower thought processes.

Heart Health Improves With Hormone Replacement

Heart Health Improves With Hormone Replacement

Conclusion

Seven major hormones have been reviewed here that all have a bearing on the risk of developing a heart attack. It is important that these hormones are balanced, so they can work with each other. Hormones can be compared to a team that works together and is responsible for our health. If one or several of the team players are ineffective, our health will suffer. For this reason hormone replacement is crucial. Hormones have effects on mitochondria of the heart muscles cells. They stabilize the heart rhythm as in the case of estradiol. But they can also strengthen the heart muscle directly through DHEA and estrogens in women and DHEA and testosterone in men. Thyroid hormones are another supportive force for the heart and can even be used therapeutically in chronic heart failure patients. When people age, many hormones are produced less, but blood tests will show this. Replacing hormones that are missing can add years of active life.

Taking care of the symphony of hormones means you are taking care of your most important organ, the heart!

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Feb
11
2017

Genetic Switches To Treat Obesity And Diabetes

Dr. Michael Nova gave a talk recently about the role of genetic switches to treat obesity and diabetes. The talk was given as part of the 24th Annual World Congress on Anti-Aging Medicine (Dec. 9-11, 2016) in Las Vegas that I attended. The full title of the talk was “Nutritional Genetics and Epigenetics in Diabetes and Obesity Management”. Dr. Michael Nova is the Chief Innovation Officer at Pathway Genomics, San Diego, CA 92121.

Twin studies are a powerful tool to show that longevity is both genetically caused as well as environmentally.

These types of studies have shown that a long life (longevity) has been caused by about 20% from genetics. 80% was contributed by a healthy lifestyle. There are powerful epigenetic factors that can slow down aging and that can interfere with the inflammatory process that causes heart disease, obesity and diabetes. There are specific inflammatory markers done with blood tests that detect inflammation. One of the first inflammatory markers detected was the C-reactive protein.

What diseases are caused from inflammation?

Dr. Nova showed a slide depicting MS and Alzheimer’s disease in the head. In the heart area atherosclerosis was shown to cause heart attacks and strokes. Next diabetes, lupus, obesity and irritable bowel disease were depicted. Finally there is arthritis that interferes with joint movements. All of these conditions have inflammation at the core, which leads to worsening of the conditions, if the inflammation is not stopped through nutritional or medical means.

Age-related diseases also due to inflammation

Inflammation is not only confined to these conditions. Research has shown that the following age-related diseases belong into the inflammatory category. These are: osteoporosis, depression, diabetes, cancer, neurodegenerative diseases (Parkinson’s disease, Alzheimer’s), asthma, central obesity, metabolic syndrome and cardiovascular disease. In these diseases the C-reactive protein is often up, so is the fasting insulin level. The rest of the talk concentrated on how various changes in food intake and supplements could lead to epigenetic changes that improve the patients’ conditions.

Human genetics are complicated

The speaker mentioned how complex the human genetics are, and he showed a number of slides that are too complicated to discuss here. There are unstable genes, which can become important in the development of illnesses, particularly when you don’t exercise and you eat a Standard North American diet. There are genes involved that cause diabetes, but they need environmental triggering to get expressed. Dr. Nova showed one slide that listed two genetic variants, which when activated by inflammation rendered the person positive for diabetes or heart disease. If inflammation is vigorously treated with a Mediterranean diet and Metformin, the hemoglobin A1C will decrease to less than 6.0% and diabetes will disappear.

Obesity and genetic factors

Obesity has a 40% to 60% hereditary rate. The fat mass and obesity-associated gene, FTO gene for short is the reason some people gain weight. When this gene is not present the person has no problem maintaining a normal weight. The FTO gene is located on chromosome 16. There are other genes with complicated names that can also increase weight.

It is important that there are many factors that work together in developing obesity. Dr. Nova called this the “epigenetic modulation”. He explained further that there are at least 12 factors working together that can reduce obesity. These are:

  1. Diet
  2. Diurnal/seasonal correlations
  3. Smoking and other toxic chemicals
  4. Street drug use
  5. Disease exposure
  6. Financial status
  7. Exercise status
  8. Microbiome healthy?
  9. Therapeutic drugs
  10. Alternative medicine
  11. Social interactions
  12. Psychological state

Low carbohydrate diets and the ketogenic diet are helping to reduce weight. Financial stress leads to more cortisol production, which leads to weight gain. An unhealthy bacteria composition in your gut causes you to gain weight, while a good composition of bacteria helps you lose weight. Overcoming depression with cognitive therapy can help reduce your weight. Those are just a few examples in more detail from the list of 12 factors.

Extensive research has shown that genetic factors and environmental factors interact to lead to epigenetic marks or imprinting. These epigenetic factors have an influence on gene expression, but they don’t change the underlying DNA sequencing.

There are still gaps of knowledge how obesity develops, what percentage is due to genetic factors and how much is due to other factors including diets.

Diabetes and genetic factors

Major metabolic processes in our body cells like phosphorylation, acetylation and methylation can be influenced by nutrition. This allows epigenetic mechanism of actions to interfere with the expression of inherited health problems like diabetes and other diseases. This has the potential to improve quality of life.

Useful supplements

Dr. Nora showed a slide with a number of useful supplements.

  • EGCG is the effective component of green tea. It supports the viability of the beta-islets of the pancreas that produce insulin. It leads to more secretion of insulin.
  • Naringin and Hesperidin decrease high blood sugar levels.
  • Anthocyanin decreases high blood sugar levels.
  • Quercetin increases cell proliferation in the liver and the pancreas.
  • Vitamin D3 reduces diabetes incidence and inflammation of the insulin-producing cells.
  • Biotin in combination with chromium increases insulin secretion and lowers blood sugars.
  • Vitamin B2, also known as riboflavin has anti-inflammatory effects.
  • Alpha-lipoic acid protects against diabetes by reducing blood sugar levels.

There are several genes involved in the development of type 2 diabetes, one of them is the FTO gene that is also involved in the development of obesity. But Dr. Nora projected a slide that showed 14 other genes that can be involved in the development of diabetes. I have elected to not get into all of those details.

What Dr. Nora concluded is the fact that nutrition could play a vital role in preventing these genes from being expressed. He talked about silencing genes, which good nutrition and supplements can do.

Silencing diabetes genes

A Mediterranean diet can stabilize the metabolism and fight inflammation. Zinc and magnesium are important cofactors in enzymes necessary to prevent diabetes. Vitamin D3 and omega-3 intake are helping to control inflammation and preserve beta cells in the pancreas in diabetes patients.

Nutritional genetic modifiers are

Foods that methylate DNA and silence genes are: citrus (hesperidin), apples (phloretin) and tomatoes (lycopene). The following foods do both DNA methylation and histone modifications: turmeric (curcumin), cinnamon (coumaric acid), green tea (EGCG), soybean (genistein), coffee (caffeic acid) and broccoli (isothiocyanates). These three foods only do histone modifications: garlic (allyl mercaptan), grapes, (resveratrol) and cashew nuts (anacardic acid).

Functional foods with regard to obesity and diabetes

Here are a few food items and their effects on your health.

  • The lignans of flaxseed lower LDL cholesterol and total cholesterol.
  • The catechins of green tea prevent obesity, but also obesity-induced type 2 diabetes.
  • Saponins of fenugreek lower lipid peroxidation and increase the antioxidant level.
  • Soy proteins contain phytoestrogen, genistein and daidzein; this lowers cholesterol levels in the blood, prevents lipid peroxidation and has antioxidant activity.
  • Banaba leaves extract contains corosolic acid and ellagitannins. These substances are able to lower glucose levels in the blood. It also has an anti-obesity effect.
  • Grapes and related products contain anthocyanin, flavan-3-ols and flavonols. They have blood pressure lowering qualities, lower blood fat levels and prevent hardening of the arteries.
  • Dark chocolate contains flavanols that are the main type of flavonoid found in it. Flavanols decrease blood pressure and make platelets in the blood less sticky. This prevents heart attacks and strokes. In addition LDL cholesterol is decreased.
  • Red wine, berries, pears, and apples: proanthocyanidins are the active polyphenols that make all of these fruit valuable. The antioxidant effects of proanthocyanidins prevent LDL to get oxidized, which in turn slows down hardening of the arteries. It reduces the inflammation associated with narrowing of blood vessels and normalizes the lining of arteries.
  • Onions contain two active ingredients, allyl propyl disulfide (which makes you cry when you cut onions) and S-methyl-cysteine sulfoxide. These substances have anti-diabetic effects and lower blood fatty substances.
  • Turmeric contains curcumin, which possesses antidiabetic properties.
  • Fruit and vegetables contain fiber, which lowers blood sugars and hemoglobin A1C.
  • Stevia from the stevia plant reduces blood sugars following a meal in patients with type 2 diabetes.

In summary, all these substances are examples of triggering epigenetic mechanisms to interfere with the expression of negative inherited health problems.

Genetic Switches To Treat Obesity And Diabetes

Genetic Switches To Treat Obesity And Diabetes

Conclusion

This was a whirlwind review of how genetic and epigenetic traits can be overcome by a healthy diet, by supplements, fruit and vegetables, exercise and other healthy lifestyles. After reading about this huge line-up of substances that can contribute to your health, you may feel slightly overwhelmed. Are you going to get all these wonderful items from the health food store and live on a bunch of supplements? Of course this is not the fact! Some herbals can be extremely helpful to combat inflammation, such as curcumin. But the most essential fact remains very simple: to cut down sugar and too many starchy foods, as they will trigger suppressed genes to cause diabetes, obesity, heart attacks and strokes. We need to inform ourselves and stay vigilant to the fact how toxic processed foods are, and we have to cut them out in order to stay healthy. We can become much more resilient to health challenges than we may have thought possible.

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Feb
04
2017

Benefits Of The Ketogenic Diet

Dr. Jeff Volek, PhD, RD gave a talk that clarified the benefits of the ketogenic diet. He is a professor at the Department of Human Sciences at The Ohio State University, Columbus, OH, and teaches in the Kinesiology Program. His lecture was part of the 24th Annual World Conference on Anti-Aging Medicine in Las Vegas, Dec. 9 to 11, 2016.

There were 58 slides, some of them very detailed. I will summarize as best as I can what the presentation was all about.

History of diets

Dr. Volek stated that there were unintended consequences when the low fat/ high carb diet was introduced in the 1970’s and 1980’s. Ancel Keys, a physiologist had proposed in his diet heart hypothesis that saturated fat was the culprit that caused heart attacks.

As a result all major health agencies recommended the low fat/high carb diet. Obesity, diabetes, heart attacks, and strokes were the consequences. Another offshoot later from this was the statin craze where everybody was put on statins as high cholesterol was symptomatically treated. Nothing changed the diabetes and obesity wave and heart attacks and strokes continued to kill the affected persons. Among performance athletes the hypothesis was formed that carb loading would increase muscle performance. Researchers showed evidence that carb loading would improve performance. But athletes were dissatisfied with prediabetes and metabolic problems. Both the average consumer as well as the performance athlete noted that they felt better on a low carb/high fat diet. This is what the ketogenic diet is all about.

Diet heart hypothesis

With the diet heart hypothesis the saturated fat was removed from the diet and replaced by vegetable oils rich in linoleic acid. Dr. Volek explained that blood tests and other investigations were done on people who ingested the low saturated fat/high carb diet. The question was whether this would reduce heart attack rates and deaths by lowering serum cholesterol.

The Minnesota Coronary Experiment was a double blind study, which answered this question.

Cholesterol was reduced in the experimental group. But there was no reduction of heart attacks or strokes compared to a control group. Of concern was the large amount of refined carbohydrate content with the low fat diet. This essentially was responsible for the obesity and diabetes wave. The excess sugar turned into fat deposits and to insulin resistance, which caused diabetes. The low saturated fat/high carb diet of the 1960’s to 1990’s did not reduce heart attacks and strokes. To the contrary: the obesity/type 2 diabetes wave it had caused increased mortality from strokes and heart attacks further.

Laboratory tests on low fat/high carb diet versus the ketogenic diet

Forget hypotheses for a moment. Let us review what the different diets do in terms of lab tests. In a study where 40 overweight people with metabolic syndrome were put on a low fat diet or a low carb/ketogenic diet, the following blood test results were found. There were 20 patients in each group.

  1. Low fat/high carb diet

Triglycerides in the blood went down by 20%, saturated fatty acids by 22%. LDL (the bad cholesterol) rose by 4%. Insulin levels went down by 17% and leptin levels also down by 17%. Glucose levels were down by 1%.

  1. Low carb/ketogenic diet

Triglycerides went down by 52%, saturated fatty acids by 57%. LDL (the bad cholesterol) went down by 18%. Insulin levels went down by 49% and leptin levels by 42%. Glucose levels were down by 11%.

In this group of 20 subjects for each group the body mass index went down by 5% for the low fat diet and by 10% for the ketogenic diet after 3 months. The abdominal fat went down in that time by 12% for the low fat diet and by 20% for the ketogenic diet. The conclusion from these laboratory results and from the body measurements is that the low fat diet is showing some results of weight loss, but the ketogenic diet has superior results. The same is true for the blood tests. Only the ketogenic diet showed reduction of 7 key anti-inflammatory markers. In contrast, the low fat diet did not trigger the production of a single anti-inflammatory marker.

Anti-inflammatory benefits of the ketogenic diet

A 2008 study showed that several anti-inflammatory markers were greatly reduced from the ketogenic diet while a low fat diet did not show such a reduction.

As this 2009 study showed the LDL particles were getting bigger under the influence of a ketogenic diet, but they were getting smaller with a low fat diet.

Large LDL particles are also called pattern A particles, while small LDL particles are also called pattern B particles.

As this link shows there is good evidence that small LDL particles oxidize easier and are more atherogenic (causing hardening of the arteries). This means they lead to hardening of the arteries easier translating into heart attacks and strokes down the road. It is one thing that a ketogenic diet leads to larger LDL particles, which are more resistant to oxygenation. But it is another good thing that this diet is also anti-inflammatory. Overall this means that a ketogenic diet is counteracting the development of heart attacks and strokes.

Are saturated fatty acids in the diet causing heart attacks or strokes?

Dr. Volek discussed several large studies that have investigated this question. One of these studies discussed was a metaanalysis from 2010. Like all the other studies it showed that saturated fatty acids do not cause heart attacks and strokes. This is the secret behind the Inuit and the Eskimo diet. It is a high fat and meat diet. Lots of seafood is consumed as well, which provides omega-3 fatty acids.

Dr. Volek pointed out that if you replace a certain percentage, let’s say 5% of saturated fatty acids with carbohydrates, this would cause 7% more heart attacks. He showed literature evidence to back this up. What causes increased heart attacks and strokes is more refined carbs in your diet (sugar and starchy foods!).

Do saturated fatty acids in your blood increase the risk for disease?

Dr. Volek showed several slides with references to various publications. Elevated saturated fatty acids in the blood cause a higher risk of getting a heart attack, heart failure, metabolic syndrome and diabetes. But this does not happen with a ketogenic diet. The values of the saturated fatty acids in the blood are 4% lower when a ketogenic diet is started. With a low carb diet the calories derived from carbs are 12%. In comparison a low fat diet has 56% of carbs. Protein content in the low fat diet is 20%, in the ketogenic diet 28%. Saturated fat content in the low fat diet is 24%, in the ketogenic diet it is 59%. Let’s assume that both diets are kept at 1500 Cal. per day. Then the saturated fat content for the low fat diet is 12 grams and the carbohydrate content is 208 grams. For the ketogenic diet these values are as follows: 36 grams of saturated fat and 45 grams of carbohydrates. Despite a threefold higher saturated fatty acid intake the circulating level of saturated fatty acids in the blood were decreased by 4%.

You are what you eat, but go easy on carbs

Dr. Volek pointed out that what makes you healthy or sick is how many carbs you include in your diet. If you follow a ketogenic diet with only 12% carbs you are much better off than when you follow a diet like the low fat diet with 56% of carbs. The higher the carb percentage in your food, the higher the production of saturated fatty acids in your system and the higher the storage of saturated fatty acids in your body fat. Conversely, the lower the carb percentage in your food is the higher the oxidation of saturated fatty acids will be. In other words the saturated fatty acids disappear from your blood. Also, with a ketogenic diet the storage of saturated fatty acids is lower in your body fat. With a low fat diet your insulin resistance increases, while with a ketogenic diet insulin resistance decreases. The difference in calories in these two diets (56% derived from carbs in a low fat diet versus 12% derived from carbs in a ketogenic diet) explains why the obesity/type 2 diabetes wave has developed and why heart attacks and strokes still top the mortality figures today.

Endurance athletes win medals on a ketogenic diet

Dr. Volek shared a few cases of world-class athletes that are on a ketogenic diet. They did well for themselves winning medals. Tim Olsen won the Western States 100-mile endurance run from Squaw Valley to Auburn, CA in 2012. Zach Bitter was the 100-mile track record holder in 2015. Mike Morton won the American 24-hour distance running record for 172 miles. Two Tour De France bicyclists made first and second place, Chris Froome (first place) and Romain Bardet (second place).

Sports teams also have been successful on a ketogenic diet: the Columbus Crew soccer team; New Zealand national rugby union team, commonly called the All Blacks; the Los Angeles Lakers basketball team are all on ketogenic diets.

Dr. Volek also pointed out that the ketogenic diet has even been tested for the military. A ketogenic diet restores metabolic health, gives the soldiers more endurance, more stress resistance and decreased fatigue.

Benefits Of The Ketogenic Diet

Benefits Of The Ketogenic Diet

Conclusion

A ketogenic diet is on the one end of the carb spectrum with only 10 to 12% of calories derived from carbs. At the other end is the low fat/high carb diet that caused the obesity/diabetes wave. The Mediterranean diet is in the center. The more you are able to cut down the carb percentage in your diet by cutting out sugar and starchy foods, the more your metabolism gets stabilized and this can be measured with blood tests. The ketogenic diet makes you lose weight down to your ideal weight and makes you gain more muscle strength and physical endurance. Sophisticated blood tests have shown that inflammatory markers go down on a ketogenic diet and factors that lead to hardening of arteries also go down. The end result on the ketogenic diet is that the rate of heart attacks and strokes goes down, something which was the original goal of Ancel Keys. It did not work, but it promoted a wave of diabetes and heart disease! Ironically adding saturated fat and other healthy fats while cutting down carbs will achieve disease prevention. This is the opposite of what Ancel Keys had recommended to do and what the processed food industry has mimicked. The ketogenic diet lowers mortality by cutting down heart attacks and strokes. With this knowledge it will finally be possible to get people on a path to better health.

More information about ketogenic diet: https://www.dietdoctor.com/low-carb/keto

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Jan
28
2017

Cardiovascular Disease And Inflammation

Dr. Mark Houston talked about cardiovascular disease and inflammation – “the evil twins”. He presented this lecture at the 24th Annual World Congress on Anti-Aging Medicine (Dec. 9-11, 2016) in Las Vegas. Dr. Houston is an associate clinical professor of medicine at the Vanderbilt University Medical School in Nashville, TN 37232.

New thinking about cardiovascular disease and inflammation

Dr. Houston pointed out that the old thinking about cardiovascular disease has to be replaced with the new thinking. Here are a number of points regarding the new thinking.

  1. Coronary heart disease and congestive heart failure are diseases of inflammation. They are also coupled with oxidative stress, vascular immune dysfunction and dysfunction of the mitochondria.
  2. In the past it was difficult to reduce these cardiovascular diseases. With the new thinking there are now new treatment approaches that help cure cardiovascular disease.
  3. The development of heart disease has a long history. Endothelial dysfunction predates coronary artery disease by many years. This is followed by vascular smooth muscle dysfunction. Inflammation develops and structural changes occur in the small and larger blood vessels with atheromatous deposits (plaques) and final occlusion, at which point you get a heart attack.

Canadian physician Sir William Osler has already stated more than 100 years ago “A man is as old as his blood vessels”.

The old thesis was that cholesterol would lead to deposits that close coronary blood vessels and cause heart attacks. Dr. Houston called this the “cholesterol-centric “ approach. The truth is that with conventional blood tests you are missing 50% of all the high-risk patients that are going to develop heart attacks. They are missing the ones that have chronic inflammation, but normal cholesterol levels.

What was not known in the past was that oxidative stress associated with normal aging can lead to chronic low-grade inflammation. This oxidative stress leads to mitochondrial DNA changes. Associated with it are biochemical changes that cause chronic inflammation, which in turn will affect the lining of the arteries. There is a metabolic change described in the literature as metabolic syndrome, which leads to high blood pressure, hardening of the arteries and eventually heart attacks and strokes. The key today is to include in screening tests all parameters that will predict who is at risk to develop a heart attack or not.

Blood tests to screen for cardiovascular disease and inflammation

Blood tests and health history should be checked for dyslipidemia, high blood pressure (hypertension), hyperglycemia, smoking, diabetes, homocysteinemia, obesity etc. Also, patients with high GGTP (gamma-glutamyl transferase) levels in the blood are more at risk to develop diabetes. This in turn leads to inflammation of the arterial wall and heart attacks. There are 25 top risk factors that are associated with all causes for heart attacks.

Briefly, apart from the 7 factors already mentioned above the physician wants to check for high uric acid levels (hyperuricemia), kidney disease, high clotting factors (fibrinogen levels), elevated iron levels, trans fatty acid levels, omega-3 fatty acid levels and omega-6 to omega-3 ratio, low dietary potassium and magnesium intake with high sodium intake, increased high sensitivity C reactive protein level (hs CRP measuring inflammation). The list to test for cardiovascular disease risk continues with blood tests for vascular immune dysfunction and increased oxidative stress, lack of sleep, lack of exercise, subclinical low thyroid levels, hormonal imbalances for both genders, chronic infections, low vitamin D and K levels, high heavy metals and environmental pollutants.

The speaker stated that he includes a hormone profile and vitamin D levels. He does biochemical tests to check for mitochondrial defects. Micronutrients are also checked as cardiovascular patients often have many nutritional deficiencies. Inflammation is monitored through testing the levels of C-reactive protein (CRP).

In order to assess the risk of a patient Dr. Cohen, a cardiologist has developed the Rasmussen score, which is more accurate than the Framingham score.

The following tests are performed on the patient: computerized arterial pulse waveform analysis (medical imaging), blood pressure at rest and following exercise and left ventricular wall of the heart by echocardiography. Further tests include urine test for microalbuminuria, B-type natriuretic peptide (BNP, a measure of congestive heart failure), retinal score based on fundoscopy, intima-media thickness (IMT, measured by ultrasound on the carotid artery) and electrocardiogram recording (EKG).

Here is what the Rasmussen score means:

  • Disease score 0 to 2: likely no heart attack in the next 6 years
  • Disease score 3 to 5: 5% likely cardiovascular events in the next 6 years
  • Disease score > 6: 15% likely cardiovascular events in the next 6 years

Non-intervention tests to measure cardiovascular health

1. The ENDOPAT test

With this test the brachial artery is occluded with a blood pressure cuff for 5 minutes. Endothelial dysfunction is measured as increased signal amplitude. A pre- and post occlusion index is calculated based on flow-mediated dilatation. The values are interpreted as follows: an index of 1.67 has a sensitivity of 82% and specificity of 77% to predict coronary endothelial dysfunction correctly. It also correlates to a future risk for coronary heart disease, congestive heart disease and high blood pressure.

2. The VC Profile

This test measures the elasticity of the arteries. There is a C1 index that measures the elasticity of the medium and smaller vessels and the C1 index, which measures elasticity of the larger arteries and the aorta. The smaller the numbers are, the less elastic the arterial walls.

3.The Corus CAD score

This is a genetically based blood test. The score can be between 0 and 40. If the score is 40, there is a risk of 68% that there is a major blockage in one or more coronary arteries.

4. Coronary artery calcification

The CAC score correlates very well with major event like a heart attack. There is a risk of between 6- and 35-fold depending how high the CAC score is. The key is not to wait until you have calcification in your coronary arteries, but work on prevention.

Treatment of cardiovascular disease and inflammation

When heart disease is treated the doctor needs to address all of the underlying problems. It starts with good nutrition like a DASH diet or the Mediterranean diet.

Next anti-inflammatory and other supplements are added: curcumin 500 mg to 1000 mg twice a day, pomegranate juice ¼ cup twice per day, chelated magnesium 500 mg twice per day, aged garlic 1200 mg once daily, taurine 3 grams twice per day, CoQ-10 300 mg twice per day and D-ribose 5 grams three times per day. This type of supplementation helps for chest pain associated with angina. On top of this metabolic cardiology program the regular cardiac medicines are also used.

Additional supplements used in the metabolic cardiology program may be resveratrol 500 mg twice per day, quercetin 500 mg twice per day, omega-3 fatty acid 5 grams per day, vitamin K2 (MK 7) 100-500 micrograms per day and MK4 1000 micrograms per day. In addition he gives 1000 mg of vitamin C twice per day. This program helps in plaque stabilization and reversal and reduction of coronary artery calcification.

Case study showing the effect of metabolic cardiology program

Here is a case study of a heart patient that was treated by Dr. Houston. He was a white male, first treated for congestive heart failure as a result of a heart attack in June 2005. Initially his ejection fraction was 15-20%. His medications were: digoxin 0.25 mg once daily, metoprolol 50 mg twice per day, ramipril 10 mg twice per day, spironolactone 25 mg twice per day and torsemide 20 mg once daily. These medications were kept in place, but the metabolic cardiology program was applied in addition. Here are the results of his ejection fraction (EF) values after he was started on the metabolic program:

  • Initial measurement: EF15-20%. Marked shortness of breath on exertion.
  • 3 months: EF 20-25%. He reported improved symptoms.
  • 6 months: EF 25-30%. He said that he had now minimal symptoms.
  • 12 months: EF 40%. He had no more symptoms.
  • 24 months: EF 50%. He reported: “I feel normal and great”.
  • 5 years: EF 55%. He said” I feel the best in years”.

A normal value for an ejection fraction is 55% to 70%.

Cardiovascular Disease And Inflammation

Cardiovascular Disease And Inflammation

Conclusion

Testing for heart disease risk has become a lot more sophisticated than in the past, and the tests have opened up a window to early intervention. Metabolic cardiology is a new faculty of cardiology that assists in the reversal and stabilization of heart disease. It will help high blood pressure patients and stabilizes diabetes, which would otherwise have deleterious effects on heart disease. Metabolic cardiology improves angina patients. It also prevents restenosis of stented coronary arteries. As shown in one clinical example reduced ejection fractions with congestive heart failure will improve. This was achieved solely through the metabolic cardiology program.

As usual, prevention is more powerful than conventional treatment later. To give your cardiac health a good start, don’t forget to cut out sugar, exercise regularly and follow a sensible diet.

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Jan
21
2017

Effects Of Metformin On The Gut Microbiome

Matthew Andry, MD talked about the effects of metformin on the gut microbiome. This talk was delivered at the 24th Annual World Congress on Anti-Aging Medicine. The congress took place from Dec. 9 to Dec. 11, 2016 in Las Vegas. A lot of the sessions that I attended dealt with the gut flora and how it affects our health. This talk belongs to the theme of what a healthy gut microbiome can do for us.

History of metformin

Dr. Andry is a clinical associate professor of the Indiana School Of Medicine.

He pointed out that metformin has been used for a long time for type 2 diabetes, particularly, if fasting insulin levels are high. Metformin is a biguanide, which was isolated from French lilac (also known as Goats Rue). In the middle ages this herb was used to treat “thirst and urination”. In retrospect we recognize these as symptoms of diabetes. Chemists were able to synthesize the active ingredient in this herb in the 1920’s. Since then it is known as metformin. Dr. Jean Stern was able to show in the 1950’s in clinical studies that Glucophage, the brand name of metformin was able to reduce blood sugar without raising insulin levels. Between 1977 and 1997 metformin enjoyed wide spread acceptance for treating diabetics. Several clinical investigators demonstrated that diabetic patients on metformin lived longer and had less heart attacks than patients who were treated otherwise.

Metformin is the first-line drug in the treatment of type 2 diabetes in children and adults. It is one of the most widely prescribed drugs throughout the world with 120 million prescriptions per year.

Off-label use of metformin

There are many other clinical conditions for which metformin have been found to be beneficial. Polycystic ovary syndrome (PCOS), obesity, prediabetes, metabolic syndrome and nonalcoholic steatohepatitis are a few examples of off-label use of metformin. Metformin is also used as an anti-aging agent as it was found to elongate telomeres, which helps people to live longer. Metformin has been identified as a possible cancer prevention agent. In prostate cancer it was found to have an effect against prostate cancer stem cells. Without these cells prostate cancer does not recur after surgical removal.

Action of metformin

Metformin increases the action of an enzyme, AMPK, which leads to lipid oxidation and breakdown of fatty tissue (catabolism). In the liver the metabolic pathway of making sugar from fatty acids, called gluconeogenesis is inhibited. Metformin causes increased uptake of sugar into skeletal muscle tissue. This is the reason for the previously mentioned stabilization of blood sugar. Metformin has two beneficial effects on the liver. First it stabilizes insulin sensitivity. This means that a given amount of insulin has a larger effect on the liver. Secondly metformin decreases the toxic effect of fatty acids on the liver tissue. In other words metformin has a healing effect on non-alcoholic steatohepatitis, a precursor to fatty liver and liver cirrhosis. Metformin also has an effect on the appetite center in the brain. It helps many obese and overweight people, but not all to lose weight. The mechanism for that effect is in the hypothalamus, where the appetite center is located. The neuropeptide Y gene expression in the hypothalamus is inhibited by metformin leading to reduced appetite.

Finally, metformin also normalizes the gut flora. This last point was the main focus of Dr. Andry’s talk.

Metformin and the gut

An animal experiment on mice showed in a study published in 2014 that metformin was stimulating the growth of a beneficial gut bacterium, Akkermansia. This is a mucin-degrading bacterium. But it also affects the metabolism of the host. The authors found that metformin increased the mucin-producing goblet cells.

Akkermansia muciniphila bacteria were fed to one group of mice. This group was on a high fat diet, but not on metformin. The mice showed control of their blood sugars, as did the metformin group. In other words manipulation of the gut flora composition could achieve control of the diabetic metabolism. The authors concluded that pharmacological manipulation of the gut microbiota using metformin in favor of Akkermansia might be a potential treatment for type 2 diabetes.

Effect of metformin on the gut flora

Akkermansia muciniphila bacteria comprise 3%-5% of the gut flora. It does not form spores and is strictly anaerobe, in other words oxygen destroys it. This is the reason why it is difficult to take it as a supplement. It is mostly growing in the mucous of the epithelium layer of the gut. The highest number of Akkermansia bacteria is found in the colon, lesser amounts in the small intestine of all mammalian species including the human race.

Here are the effects of metformin on Akkermansia:

  • Metformin increases the Akkermansia bacteria count both in a Petri dish as well as in the gut of experimental mice. This suggests that metformin acts like a growth factor for Akkermansia.
  • Metformin increased the count of Akkermansia bacteria by 18-fold up to a maximum of 12.44% (up from the normal 3-5%) of all of the gut bacteria.
  • Researchers observed that the mucin layer of the lining of the gut in metformin treated mice was thicker. This suggests that the thickness of the mucin layer plays a role in increasing the Akkermansia count.

Effect of the gut on the body’s metabolism

Other researchers have investigated how a high fat diet can change the composition of the gut bacteria, which in turn are altering the body’s metabolism. Essentially a shift in the bowel flora can increase the gut’s permeability. This is called leaky gut syndrome. It leads to absorption of lipopolysaccharides (LPS) from bad bacteria in the gut. The end result is endotoxemia in the blood. This causes systemic inflammation in the body. Insulin resistance and obesity develop and this can be followed by type 2 diabetes. It is interesting to note that the effects of a high fat diet that led to these changes can be reversed by increasing Akkermansia bacteria in the gut or by treating with metformin.

An interesting mouse experiment showed that the changes that take place in the gut bacteria with cold exposure could be transferred to germ-free mice with no gut flora. This changed their metabolism proving that gut bacteria have profound influences on the metabolism. The fact that the gut bacteria have a profound influence on the metabolism is not only true for animals, but also for humans.

Akkermansia Facts

Here are a few facts about the Akkermansia bacteria.

  • The amounts of Akkermansia bacteria in the gut are inversely related to how fat we are. This is measured by the body mass index (BMI). Fat people have less Akkermansia in their guts.
  • A high fat diet lowers the amount of Akkermansia in the gut
  • Systemic inflammation is present with low Akkermansia counts
  • A high fat diet causes gut permeability (leaky gut syndrome).
  • Low levels of Akkermansia causes worsened severity of appendicitis and inflammatory bowel disease.
  • Low levels of Akkermansia causes fat storage (both in subcutaneous fat and visceral fat).
  • Low levels of Akkermansia cause insulin resistance (associated with diabetes) and high blood sugars.
  • Increased Akkermansia counts increase brown fat’s ability to burn calories, which leads to weight loss. Decreased Akkermansia counts lead to fat storage (weight gain).
  • Increased Akkermansia improves gut-barrier integrity
  • Increased Akkermansia reduces visceral and total body fat
  • Increased Akkermansia reduces synthesis of sugar in the liver (gluconeogenesis)

We have 10 times more bacteria in the gut than we have cells in our body. The Akkermansia percentage of the gut flora can be decreased from antibiotics or food that contains traces of antibiotics. If there is a lack of Akkermansia species, there is more gut permeability, causing LPS increase and causing increase of inflammation in the body. This translates into high blood pressure, heart attacks, strokes, and degenerative neurological diseases like Parkinson’s disease, Alzheimer’s disease or MS. But it can also cause inflammatory bowel disease and autoimmune diseases.

What increases Akkermansia?

We can increase Akkermansia bacteria in the gut by eating Oligofructose-enriched prebiotics. Oligofructose belongs into the inulin type soluble fibers. It is found in a variety of vegetables and plants. This includes onions, garlic, chicory, bananas, Jerusalem artichokes, navy beans and wheat. But wheat can be problematic. Clearfield wheat is the modern wheat variety which is now grown worldwide. It is much richer in gluten and can cause problems with gut permeability.

Eating lots of vegetables and fruit will give you enough of oligofructose to maintain a healthy percentage of Akkermansia in your gut bacteria.

Metformin as pointed out earlier can be used as pharmacotherapy. But it must be stressed that the use of metformin for dysmetabolic syndrome is off-label. There are real side effects of metformin. Lactic acidosis with an unusual tiredness, dizziness and severe drowsiness can develop. Also chills, muscle pain, blue/cold skin and fast/difficult breathing has been described. Slow/irregular heartbeat, vomiting, or diarrhea, stomach pains with nausea are also listed under side effects.

Effects Of Metformin On The Gut Microbiome

Effects Of Metformin On The Gut Microbiome

Conclusion

Our gut bacteria are important for us, more so than you may be aware of. An anaerobe bacterium, Akkermansia makes up 3%-5% of the gut flora. This bacterium lives in the mucous layer of the lining of the gut and ensures that the gut wall is tight. When these bacteria are lacking (due to consumption of junk foods) the gut wall becomes leaky, which is why this condition is called “leaky gut syndrome”. Irritating toxic substances can now leak into the blood stream and lipopolysaccharides are among them. This causes inflammation in the gut wall, but can go over into the blood vessels and the rest of the body including the brain. High blood pressure, obesity, diabetes, heart attacks, strokes, and degenerative neurological diseases like Parkinson’s disease, Alzheimer’s disease or MS can develop from the inflammation. But it may also cause inflammatory bowel disease and autoimmune diseases.

Eating lots of vegetables and fruit will give you enough of oligofructose to maintain a healthy percentage of Akkermansia in your gut bacteria. In particular, onions, garlic, chicory, bananas, Jerusalem artichokes and navy beans provide lots of oligofructose to support Akkermansia in your gut bacteria.

As pointed out earlier metformin can be used as pharmacotherapy of dysmetabolic syndrome. But it must be stressed that the use of metformin is off-label. It is also important to remember, that with effects there are side effects of metformin.

It may be news to you, how close the health of the gut is connected to our overall health. With the knowledge that food can be your medicine, choose your foods wisely. Add some or all of the above named foods that help you support beneficial gut bacteria, and take care of your health!

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Jan
14
2017

How To Avoid Being Hungry

Dr. Ludwig gave a lecture about how to avoid being hungry at a conference in Las Vegas. The actual topic was “Always Hungry?” I attended the 24th Annual World Congress on Anti-Aging Medicine (Dec. 9-11, 2016) in Las Vegas where this lecture was given. Dr. Ludwig is a Harvard-based endocrinologist who has been researching weight loss methods and obesity for over 20 years. Here is a list of his major publications.

Dr. Ludwig stated that the low fat/high carb diet popular in the1980’s until the early 2000’s was misguided and probably even harmful. The theory at that time was that obesity was caused by too much saturated fat. This has since been proven to be wrong. Instead it has been proven that increased sugar intake is responsible for the obesity wave.

General information about weight gain

The carbohydrate-insulin model states that without insulin you cannot gain weight, because in order to store fat in fatty tissue you need insulin to transport fatty acids across the cell membrane of fat cells.

In this context it is important to note that high glycemic index food increases the blood sugar. This leads to stimulated insulin production, and the liver converts the extra sugar into fatty acids that get deposited as fat in fatty tissue.

The glycemic load from a person’s diet is the single best predictor for a rising blood sugar level. After food intake the blood sugar goes up, glucagon goes up, epinephrine goes up within 4 hours. It is the epinephrine, which after 4 hours makes you hungry again.

The nucleus accumbens is the addiction center. At 4 hours after a high glycemic index milk shake the nucleus accumbens was stimulated in 12 subjects of a double blind trial.

The nucleus accumbens does not work in isolation. It is not only involved in food satisfaction, but also in sexual satisfaction and even plays a role in satisfaction that some people get from playing video games.

Low-carbohydrate, Mediterranean or low-fat diet

In an Israeli study from the New England Journal of Medicine in 2008 investigators were interested to find out which diet was helping people to lose most weight. h

322 moderately obese subjects that were aged 52 years on average were randomized to one of the following diet groups.

They compared

  1. a low fat diet (Atkins type, restricted calorie) with a
  2. Mediterranean diet (low carb, restricted-calorie) and a
  3. Low fat/high carb diet (low fat, non-restricted-calorie)

What was the result? The mean weight losses were: 2.9 kg (low fat group), 4.4 kg (Mediterranean diet group), and 4.7 kg (low fat/high carb group). Of the 272 participants who had completed the intervention after two years of the study the weight loss was 3.3 kg, 4.6 kg, and 5.5 kg in the same sequence as above.

The ratio of total cholesterol to high-density lipoprotein cholesterol, which is a measure for the heart attack risk, was examined next. It was 20% lower from the baseline in group 2 (Mediterranean diet group). The low fat groups (group 1 and 3) were 12% lower from the baseline.

36 subjects had diabetes. There was a clear winner with respect to lower fasting blood sugar and insulin levels, namely the Mediterranean diet (group 2).

The authors concluded that the Mediterranean diet is preferable to low fat diets as they have shown an improvement in lipid profiles and in control of diabetes.

The “POUNDS LOST” study

This was a 2-year study that investigated 4 different lower calorie diets to help people lose weight. Despite the significant difference in diet composition, these 811 free-living overweight or obese adults ages 30-70 from Boston, MA and Baton Rouge, LA lost 16 pounds at 6 months and 9 pounds at the end of two years. The diets were 1) low fat (20%) or 2) high fat (40%) 3) average protein (15%) or 4) high protein (25% of total calories).

The authors concluded that any reduced, calorie-controlled diet would help obese or overweight people to achieve weight loss that lasts. It is interesting that it did not matter whether the diet was low or high in fat, or had low or high protein content. What did matter was that all diets were low in sugar.

Sugar is the driving force

Dr. Ludwig pointed out that without insulin you couldn’t gain weight. High glycemic index food increases blood sugar. The glycemic load is the single best predictor to indicate whether a person will gain weight or lose weight when this food is consumed. It is an irony that in the 1980’s and 1990’s the obesity wave was created by the wrong assumption that a low fat/high carb diet would be heart healthy. We have abundant data available that show otherwise: high sugar content of food brings the calorie count up as everybody can read on the food labels.This will lead to weight increase, which has been abundantly proven. Sugar also stimulates your nucleus accumbens, the food addiction center. As you probably know it is extremely difficult to get out of this food addiction cycle unless you cut out sugar. You even need to go one step further and include many starchy foods that will within 30 minutes of digesting them turn into sugar. Your system makes no difference whether you eat a few teaspoons of sugar or two slices of white bread. The response of your pancreas is insulin, which gladly stores the fatty substances your liver made as fat.

How to get out of the vicious food cycle

As the quoted publications and many other ones have shown, it only matters that you limit your refined carb intake. You can vary the fat content and you can vary the protein content and still lose weight provided you watch the low carb intake. You also need portion control, which is a given! Study glycemic index and glycemic load sites on the Internet. The links I provided are just some examples. The more you educate yourself about carbs, the better for you. Note that many fruit and vegetables belong to the low-glycemic load/index foods. Avoid the high glycemic index foods like dates and cornflakes. Stick to low-glycemic index foods, which are less than 55. With regard to low-glycemic load food the values should be below 10.

The Mediterranean diet is a very desirable diet, which has been proven to be anti-inflammatory.

The zone diet of Barry Sears is also an anti-inflammatory diet and he summarizes this in this link.

How To Avoid Being Hungry

How To Avoid Being Hungry

Conclusion

I have summarized the content of a talk given by Dr. Ludwig. We learnt from this that sugar and refined carbs are the driving force that leads to “feeling hungry”. This stimulates your nucleus accumbens, the food addiction center. Let’s assume that a person is obese or overweight and wants to lose some weight. You need to start by being strict with yourself. Cut out sugar and high-glycemic foods. This will remove the food addiction factor that keeps you going back to the wrong, high calorie foods. You will also consume more low calorie vegetables and fruit, which have more fiber that fills you up. Once you are used to the new way of eating, there is no need to count calories. I recommend that you weigh yourself daily on body composition scales and record the results. This allows you to monitor your body mass index (BMI), your weight, your fat percentage, and your muscle percentage. Typically you will lose 2 to 3 pounds per week on such a low-calorie diet. Later the weight loss will slow down to 1 to 2 weeks per week until you reach your goal. Don’t go lower than a BMI of 21.0 to 22.0 and discuss your goal with your doctor.

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Dec
17
2016

Magnesium Is Essential To Life

Magnesium is an important co-factor in many biochemical reactions, so magnesium is essential to life.

Many diverse diseases and cancers can develop from magnesium deficiency. The key is to supplement with magnesium regularly to get more than the government recommended daily allowance (RDA). The RDA for magnesium is 420 mg a day for males and 320 mg a day for females.

In the following I will review the diseases that occur without enough magnesium on board.

A lack of magnesium can cause heart disease

In this 2014 study 7216 men and women aged 55-80 with at high risk for heart attacks were followed for 4.8 years. The risk of death from a heart attack was found to be 34% lower in the high tertile magnesium group when compared to the lower magnesium tertile group.

The protective mechanism of magnesium was found to be as follows. Magnesium counteracts calcium and stabilizes heart rhythms. Magnesium helps to maintain regular heart beats and prevents irregular heart beats (arrhythmias). It also prevents the accumulation of calcium in the coronary artery walls. This in turn is known to lower the risk of heart attacks and strokes.

Another study, which was part of the Framingham Heart Study, examined calcification of the heart vessels and the aorta as a function of magnesium intake.

There were 2,695 participants in this study. For each increase of 50 mg of magnesium per day there was a 22% decrease in calcification of the coronary arteries. For the same increase of magnesium the calcification of the body’s main artery, the aorta, fell by 12%. Those with the highest magnesium intake were 58% less likely to have calcifications in their coronary arteries. At the same time they were 34% less likely to have calcifications of the aorta.

In a Korean study a group with low magnesium levels was at a 2.1-fold higher risk of developing coronary artery calcifications compared to a group with normal magnesium levels.

Low magnesium increases your stroke risk

In a 2015 study 4443 subjects, men and women aged 40-75 were followed along.

928 stroke cases developed. The group with the highest 30% of magnesium intake was compared with the lowest 10% of magnesium intake. They had significantly lower blood pressure (7 mm mercury) and lower total cholesterol levels. They also had 41% less strokes than those with low magnesium intake.

In a 2015 study that lasted 24 years the authors investigated 43,000 men.

Those with the highest magnesium supplement had a 26% lower stroke risk. They had been compared to those with the lowest magnesium intake.

Among women low magnesium levels were shown to cause 34% more ischemic strokes than in controls.

This study was from 32,826 participants in the Nurses’ Health Study who were followed for 11 years.

It is clear from all these studies that supplementation with magnesium can prevent strokes.

Magnesium protects kidney function

This study examined 13,000 adults for 20 years to see how kidney function was dependent on magnesium levels. Those with the lowest magnesium levels had a 58% higher risk of developing chronic kidney disease. It makes sense when you consider that magnesium is needed to keep arteries healthy, blood pressure low, and blood sugars stable. In diabetics where blood sugar is not controlled kidneys develop kidney disease. This is called diabetic nephropathy. In the presence of magnesium supplementation and a low sugar diet people are less likely to develop diabetes or kidney disease.

Magnesium helps blood sugar control

A metaanalysis showed that magnesium supplementation was able to improve blood sugar control. This occurred in both diabetics and borderline non-diabetics within 4 months of supplementing with magnesium.

Magnesium has been known in the popular press to be an important factor in helping control blood sugar. Here is an article as an example.

Magnesium good for bones and teeth

Magnesium is important for calcium metabolism and this is helping your bones and teeth to stay strong. About half of the body’s magnesium is stored in bone. Teeth are the other location where a lot of magnesium is found.

Low levels of magnesium lead to osteoporosis, because one of the two structural components of bone (calcium and magnesium) is missing. In addition low magnesium causes inflammatory cytokines to increase. These break down bones. The Women’s Health Initiative showed that when daily magnesium intake exceeded 422.5 mg their hip and whole-body bone mineral density was significantly greater than in those who consumed less than 206.6 mg daily.

With regard to healthy teeth magnesium is important as it prevents periodontal disease.

This study found that there was less tooth loss and there were healthier periodontal tissues in 4290 subjects between 20 and 80.

Those who took magnesium supplements had healthier teeth.

Migraine sufferers improve with magnesium

A double blind randomized study showed that magnesium supplementation can reduce migraines. In this trial 600 mg of magnesium supplementation was used for 4 weeks.

This reduced migraines by 41.6% in the magnesium group compared to the non-supplemented control group.

Another study showed that both intravenous and oral magnesium are effective in reducing migraine headaches.

Intravenous magnesium showed effects on improving migraines within 15 – 45 minutes. The authors concluded that both oral and intravenous magnesium could be added as a supplement to other migraine treatments.

Cancer can be caused from too little magnesium

You may be surprised to hear that magnesium can even prevent some cancers. Two cancers have been studied in detail. I will limit my discussion to these two.

Pancreatic cancer

One study found that pancreatic cancer was reduced. 142,203 men and 334,999 women, recruited between 1992 and 2000, were included. After 11.3 years on average 396 men and 469 women came down with pancreatic cancer. On the male side they found that when the body mass index (BMI) was greater than 25.0 there was a 21% reduction of pancreatic cancer for every 100 mg of added magnesium per day. There were a lot of smokers on the female side, which interfered with the study as confounding factors undermined statistical validity.

In another study, the US male Health Professionals Follow-up Study was examined after 20 years of follow-up. Those with a BMI of above 25.0 on magnesium supplementation had a reduced risk of pancreatic cancer. The pancreatic cancer rate in the higher magnesium group was 33% lower than in the lower magnesium group. The higher group consumed 423 mg of magnesium daily, the lower group 281 mg per day. It is significant that in both studies it was the heavier patients who came down with pancreatic cancer. It is known that obesity is a pancreatic risk factor.

Colorectal cancer

A study done on Japanese men showed that magnesium could protect them significantly from colon cancer.

Men who consumed the highest amount of magnesium developed 52% less colon cancer over 7.9 years. They were compared to the group with the lowest 20% intake of magnesium. The women in this study did not reach statistical significance.

A study from the Netherlands examined colon cancer in patients. They found that only in patients with a BMI of greater than 25.0 magnesium did have protective effects. For every 100 mg of magnesium per day increase there was a 19% reduction of colon polyps. And there was also a 12% reduction of colorectal cancer for every 100 mg increase of magnesium per day.

Magnesium plays an important role in genome stability, DNA maintenance and repair. It also prevents chronic inflammation and reduces insulin resistance, all factors contributing to cancer reduction.

Live longer with magnesium

Consider that magnesium is the fourth most common mineral in the body. Add to this that magnesium is a co-factor of more than 300 enzymes in the body. Magnesium is required as an important co-factor in the conversion of chemical energy from food that we ingest. Magnesium is regulating blood sugar, blood vessel health and our brain electrical activity. 50% of our stored magnesium can be found in our bones, which helps the strength and integrity of them.

Because of the distribution of the enzymes that are helped by magnesium to function properly, virtually every cell in the body depends on our regular intake of magnesium.

Since the 1950’s soils are depleted of magnesium where vegetables are grown and fruit trees are raised. We simply do not get enough magnesium from food.

But chelated magnesium is freely available in health food stores. Take 250 mg twice per day, and you will have enough.

Because our metabolism slows down, there is a critical age where magnesium deficiency becomes more obvious than when we are younger. By the age of 70 there are 80% of men and 70% of women who do not get the minimum of magnesium-required amount they should get (350 mg for men and 265 mg for women).

At this age many people are on multiple drugs. For many proton pump inhibitors (PPI) are used to suppress acid production in the stomach. PPI’s have been associated with low magnesium blood levels.

This link explains that PPI’s should not be used for longer than 1 year.

Low magnesium levels accelerate the aging process on a cellular level. Low magnesium levels increase senescent cells that can no longer multiply. Some of them could cause the development of cancer. These senescent cells also can no longer contribute to the immune system. This causes more infections with an adverse outcome.

Remember to take chelated magnesium capsules or tablets 250 mg twice per day and you will be protected from low magnesium levels in your body.

Here is why we live longer with magnesium supplementation

Our blood vessels will not calcify as early; they keep elastic for longer, preventing high blood pressure. Our kidneys will function longer with magnesium, preventing end-stage kidney disease. We need our kidneys to detoxify our system! The more than 300 enzymatic reactions all over our body help that we have more energy and that cancer is prevented. When there are fewer strokes and less heart attacks this helps reduce mortality. It also helps that there is less of a risk for Alzheimer’s disease with magnesium supplementation, because insulin resistance is reduced, which has been shown to prevent Alzheimer’s disease.

The bottom line is we live longer and healthier; that is what is meant with longevity.

Magnesium Is Essential To Life

Magnesium Is Essential To Life

Conclusion

Magnesium is a key essential mineral. It balances calcium in the body and participates in many enzymatic reactions in the body as a cofactor. As long as we have enough of this mineral we won’t notice anything. It is with magnesium deficiency that things go haywire. You could get heart disease or a stroke. You could get kidney disease. You even could get pancreatic cancer or colorectal cancer. If this is not enough, magnesium deficiency can cause diabetes, osteoporosis and bad teeth. You may suddenly die with no obvious cause. But, if your magnesium blood level is balanced from regular supplements, you will carry on living and eliminate a lot of health problems.

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Nov
05
2016

Health Risks Of Night Shifts

One of the news stories in 2016 was about health risks of night shifts. The Bureau of Labor Statistics reported in 2000 that 15 million workers (16.8 % of the working population) were doing alternative shifts (night shift work mixed with daytime shifts). In 2016 they reported 14.8% were working alternate shifts. Among blacks, Asians and Latino Americans the percentage of working alternative shifts was higher, namely 20.8%, 15.7% and 16%, respectively.

Shift work is more common in certain industries, such as protective services like the police force, food services, health services and transportation.

Evidence of health risks of night shifts

There are several publications that showed evidence of health risks of night shift workers. Here is a random selection to illustrate the health risks of night shifts.

  1. A study from 2015 examined the sleep patterns of 315 shift nurses and health care workers in Iranian teaching hospitals. They found that 83.2% suffered from poor sleep and half of them had moderate to excessive sleepiness when they were awake.
  2. This South Korean study examined 244 male workers, aged 20 to 39 in a manufacturing plant. Blood tests from daytime workers were compared to night shift workers. Inflammatory markers like the C-reactive protein and leukocyte counts were obtained. Night shift workers had significantly higher values. The investigators concluded that shift workers have increased inflammatory markers. This is a sign of a higher risk of developing cardiovascular disease in the future.
  3. A Swedish study found that white-collar shift workers had a 2.6-fold higher mortality over a control group of daytime white-collar workers.
  4. Another study compared night workers in the age group of 45 to 54 with daytime workers and found a 1.47-fold higher mortality rate in the night shift workers.
  5. In a study from China 25,377 participants were included in a study that investigated cancer risk in males with more than 20 years of night shift work. They had a 2.03-fold increased risk to develop cancer compared to males working day shifts. Women with night shift work were unaffected with regard to cancer.
  6. A Polish study examined hormones and the body mass index (BMI) among 263 women who worked night shifts and 269 women who worked day shifts. When night shift workers had worked more than 15 years at nights, their estrogen levels, particularly in postmenopausal women were elevated compared to the daytime workers who served as controls. The BMI was also increased in the nighttime workers.
  7. Chronic lymphocytic leukemia (CLL): a study in Spain showed that working for more than 20 years in rotating night shifts was associated with a 1.77-fold higher risk of developing CLL. The authors noted that melatonin levels in that group were much lower than in controls that worked only day shifts. Working in straight night shifts did not show higher risks of CLL compared to daytime workers.
  8. In a Korean study from Seoul 100 female medical technologist who worked nighttime had their melatonin levels tested, which were compared to daytime workers.  They measured 1.84 pg/mL of melatonin for the nighttime workers compared to 4.04 pg/mL of melatonin in the daytime workers. The authors felt that this is proof that the diurnal hormone system has been disrupted. When the melatonin level is altered, the circadian hormone rhythm is also changed.
  9. A group of 168 female hospital employees doing rotating nightshift work in Southern Ontario hospitals were compared to 160 day workers. Cortisol production was assessed. Cortisol production in day workers and in shift workers on their day shift was similar. However, shift workers on their night shift had flatter cortisol curves and produced less cortisol. The authors felt that this disruption of cortisol production would explain why rotating night shift workers have a higher risk of cardiovascular diseases.
  10. A Danish study with female nurses followed 28,731 nurses between 1993 and 2015. Daytime nurses were compared to rotating nighttime nurses and the incidence of diabetes was measured. Night shift workers had a risk between 1.58-fold to 1.99-fold when compared to daytime workers to develop diabetes. The risk for evening shift workers was less (between 1.29-fold and 1.59-fold).

Diurnal hormone rhythm behind health risks of night shifts

Your body has its own rules. It rewards you, if you sleep 7 to 8 hours during the night, but it will penalize you severely, if you turn it upside down. The reason is our built-in diurnal hormone rhythm. A peak of melatonin regulates sleep during the night. Melatonin is released by the pineal gland (on the base of the skull) when it gets dark outside. Daytime wakefulness is regulated by the stress hormone cortisol from the adrenal glands. These two hormones inhibit each other, cortisol inhibits melatonin and melatonin inhibits cortisol. All the other hormones are also regulated according to the diurnal rhythm: testosterone is highest in the morning, human growth hormone is highest between midnight and 3 AM etc.

When you work daytime shifts, your diurnal hormone rhythm is unchanged. But if you work night time shifts, your hormones have to adapt. This is very similar to traveling east or west where you cross several time zones. Your internal diurnal hormone system has to adjust to these changes. Typically it takes 1 day to adjust to a 1-hour time zone difference.

In people who work permanent night shifts, the hormone changes stay adjusted and there is no further switching. But most employers want to be “fair” to everybody, so they introduced the rotating night shifts, which as all the publications cited above show is the worst thing you can do. It messes with your diurnal hormone rhythm, and some people never switch completely to the new hours worked. They don’t get enough daytime sleep because the kids are loud during the day etc. The rotating shift workers are running the highest risk of getting cancer, diabetes, cardiovascular diseases, obesity, cancer, leukemia, and they have low levels of melatonin.

Health Risks Of Night Shifts

Health Risks Of Night Shifts

Conclusion

When shift workers work constant night shifts, this is less stressful to our system than the more common rotating shift work. This is where you work night shifts for a period of time, then the schedule switches to day shift, and you keep on rotating. The least health risks are associated with regular daytime work. People exposed to rotating night shifts suffer from poor sleep. They have a higher risk of gaining weight, getting obese and acquiring diabetes in time. They are at a higher risk for heart attacks, strokes and cancer. All-cause mortality is about twofold higher than for workers who work day shifts.

The underlying problem seems to be a disturbance of the diurnal hormone rhythm. Normally this regulates our waking/sleeping rhythm and keeps us healthy. But with nighttime work melatonin production weakens, cortisol production is reduced and hormone rejuvenation during rest periods suffers greatly. This weakens the immune system, allows cancer to develop and leads to chronic inflammation causing cardiovascular disease and diabetes. The remedy to prevent this from happening is to catch little naps whenever you can during the day and, if at all possible, work daytime shifts permanently.

Oct
22
2016

Arthritis Drugs Can Cause Heart Failure

The British Medical Journal has published a research articles in Sept. 2016 showing that arthritis drugs can cause heart failure. This occurs particularly in elderly patients around the age of 77 years and older. This is an age where arthritis is often causing pain, and the pain is regulated with over-the-counter pills. These anti-arthritis drugs belong into the group of anti-inflammatory drugs, called NSAIDs. This stands for “non-steroidal anti-inflammatory drugs”. The study was entitled “Non-steroidal anti-inflammatory drugs and risk of heart failure in four European countries…”

Arthritis drugs can cause heart failure shows study

Adult patients above the age of 18 who started 27 different types of NSAIDs between 2000 and 2010 were followed. 92,163 hospital admissions for heart failure were noted; 8,246,403 patients who were not taking NSAIDS served as controls. There were 4 countries involved in this study providing 2.2 million patients from the Netherlands, 7.5 million from Italy, 13.7 million from Germany and 11.1 million from the United Kingdom.

Results of study

NSAID use of up to 2 weeks prior to assessment had a risk of 19% of resulting in a hospital admission for heart failure. A control group of patients who had not taken NSAIDs for at least 6 months or more had no hospital admission risk.

Seven traditional NSAIDs were found to be associated with hospital admission for heart failure. They were: diclofenac (brand name Voltaren), ibuprofen (brand name Motrin), indomethacin (brand name Indocin), ketorolac (brand name Toradol), naproxen (brand name Naprosyn or Aleve), nimesulide (brand name Mesulid and many others), and piroxicam (brand name Feldene). In addition two COX 2 inhibitors, etoricoxib (brand name Arcoxia) and rofecoxib (brand name VIOXX) were also having the same side effects.

  1. The risk for heart failure was not the same for every NSAID. The risks ranged from 1.16-fold to 1.83-fold. Specifically ketorolac had a risk of 1.83-fold, indomethacin 1.51-fold, piroxicam 1.27-fold, diclofenac 1.19-fold, ibuprofen 1.18-fold, and naproxen 1.16-fold. Translated into common language it means that ketorolac had a risk of 83% of causing a hospital admission due to heart failure. In the case of ibuprofen it was only an 18% risk.
  2. The risk for heart failure doubled for diclofenac, etoricoxib, indomethacin, piroxicam, and rofecoxib when used at very high doses. Doubling the risk means a 200% risk. Typically, when an arthritis patient has a flare-up of pain, this is the time when the NSAIDs are usually taken at a higher dose and tend to also be taken for a longer time. Some NSAIDs had a significant risk for heart failure even at a medium dose. This was the case for indomethacin and etoricoxib. The good news was that celecoxib (brand names Celebrex and Celebra) at usual doses did not lead to an increased risk of heart failure.
  3. Dose-response curves were obtained where possible. Here the researchers looked at the effect of low, medium, high and very high doses of NSAIDs in patients. Again heart failure occurrence was studied among those patients. The result clearly showed that low and medium doses of NSAIDs were fairly safe, but high and very high doses of NSAIDs caused heart failure. Etoricoxib, Piroxicam and Rofecoxib were particularly toxic in higher doses. Indomethacin was toxic at medium and high doses. An important exception to the rule was celecoxib (brand names Celebrex and Celebra), which did not cause heart failure, either at low doses or high doses. This is one of the most used NSAIDs, so it is fortunate that it does not cause heart failure.

Discussion of study

The authors of this study discussed why they believe heart failure is developing in patients who take NSAIDs. They argued that NSAIDs inhibit prostaglandin synthesis and the enzymes COX1 and COX2. This is how inflammation and pain gets inhibited, which is a good thing. But at the same time blood supply to the kidneys is reduced, kidney function is impaired, and sodium is retained. This is a bad thing as it leads to fluid retention and fluid overload of the heart resulting in heart failure. As the prostaglandin inhibition is dose-dependent, the authors said this is the reason that the heart failure rate is also dose-dependent when measured in large populations, as was done in this study. A noted exception, as already mentioned, is the popular celecoxib, which does not cause heart failure, even at high and very high doses.

Arthritis Drugs Can Cause Heart Failure

Arthritis Drugs Can Cause Heart Failure

Conclusion

This publication has a lot of statistical power as it was based on research in 4 European countries and involved almost 10 million subjects that were compared to an equally large control population. Because of the size of the study population it was possible to calculate risk ratios for NSAIDs causing heart failure for 27 different types of NSAIDs. Furthermore, the authors succeeded in quite a few cases to calculate risk factors for different concentrations of NSAIDs used. This statistical method is called a dose-response curve. It is a powerful pointer to toxicity when high doses cause heart failure, but low doses don’t.

The physician can use the information from this publication to select one of the NSAIDs that is least harmful, like celecoxib (brand names Celebrex and Celebra) and tell the patient to use the least amount possible to minimize side-effects. Many aging arthritis sufferers will benefit from this. Hopefully the FDA will review this material and shut down the use of some of the more dangerous NSAIDs or force the manufacturer to attach a black box warning about the drugs that belong into this category. You should review what your favorite NSAID is and discuss this with your physician. Perhaps print a copy of this review and take it with you, in case your health provider has not heard about it yet.

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