Nov
26
2018

Gut Bacteria Crucial To Healthy Aging

New research presented at the London Microbiome Meeting asked the question “are gut bacteria crucial to healthy aging?” Marina Ezcurra, is a Ph.D. is a researcher working at the Queen Mary University of London in the United Kingdom. She uses a nematode (round worm) model to investigate various aspects of aging. Nematodes like C. elegans provide a useful model not only for genetic work, but also for the human gut flora as well. Moreover, it allows making observations about the connection between bacterial genes and aging. Coupled with the fact that the worm has such a short lifespan, the researchers can test bacterial genes, the aging of the worm and get meaningful results in short order.

It seems like one of the research objectives was changing the nematode’s gut flora and observing life expectancy and age-related diseases.

Pathological versus healthy gut bacteria composition

Dr. Ezcurra did a couple of experiments with the nematode C. elegans as a model. She could show that the worm’s gut bacteria composition mattered. First of all, if there was a pathological composition of the gut flora, the worm did not turn as old and there were various age-related diseases that developed. Secondly, they were very comparable to human age-related degenerative diseases like Alzheimer’s disease.

Another senior author researched how genes of gut bacteria influence life expectancy

Meet Dr. Meng Wang, associate professor of molecular and human genetics, Baylor College of Medicine in Houston, TX. He did extensive genetic research on C. elegans. He used this model, because C. elegance lives only 2 to 3 weeks. This animal model is easy to manipulate. For instance, he studied the gut bacteria composition. This link explains that he tested about 4000 E.coli bacteria with various gene defects. 29 E.coli strains when deleted, increased the worms’ lifespan.12 bacterial mutants among those prevented cancer and amyloid-beta, found in Alzheimer’s disease. Some mutant bacteria caused longevity by acting on processes linked to aging.

Colanic acid is an important anti-aging factor in C.elegans

Dr. Wang joined Dr. Christophe Herman, associate professor of molecular and human genetics at Baylor, for further research. It turned out that one of the keys to longevity of the nematodes were the mutant bacteria in the gut over-producing the polysaccharide colanic acid. This allowed the nematodes to live much longer. The researchers could show further that fission and fusion processes with regard to mitochondria are important. Mitochondria are the energy packages in cells and these processes are regulated by the presence of colanic acid. As a result, if your gut has good bacteria you can grow old and escape Alzheimer’s disease and cancer.

Dr. Meng Wang said: “Of the nearly 4,000 bacterial genes we tested, 29, when deleted, increased the worms’ lifespan. Twelve of these bacterial mutants also protected the worms from tumor growth and accumulation of amyloid-beta, a characteristic of Alzheimer’s disease in humans.” 

Creating longevity with metformin, a diabetic drug

Physicians have known for some time that metformin stimulates longevity genes. This is the reason why diabetics on metformin live longer than diabetics on insulin. Dr. Ezcurra mentioned on 24 October, 2018 in her talk at the London microbiome Meeting that she had done experiments with C. elegans and metformin. Metformin reduces the risk of cancer and increases longevity in C. elegans as well as in mice (other experiments). Currently there is a clinical trial going on that investigates anti-aging under the influence of metformin in older people.

Effects of metformin on anti-aging

Metformin has the potential to target diabetes, cancer and Alzheimer’s pathologies all at once.

The anti-aging effect in humans with metformin involves the gut bacteria. Dr. Ezcurra says that this is the reason why diabetics on metformin live longer than diabetics on insulin. Metformin influences the folate bacterial metabolism of the gut flora. Other research has shown that the Akkermansia bacteria in the gut, which are good, desirable bacteria, will increase from 3-5% to 12.44% of the gut flora under the influence of metformin. Here is the discussion in detail in the following link.

Effect of gut bacteria on psychiatric diseases, obesity and diabetes

Dr. Ezcurra said that there are many studies showing that dysbiosis of the gut can lead to psychiatric diseases, Parkinson’s disease, obesity and diabetes etc.

We need to know more about whether a healthy gut flora will let us age without causing age-related diseases. Dr. Ezcurra stated: “By better understanding the links between nutrition, microbiome, and health, we can understand how the elderly can maintain their microbiome, and also help them directly by using pre- and probiotic strategies. This would help us age in a better way, maintaining health and quality of life in old age without drugs or surgery.”

Gut Bacteria Crucial To Healthy Aging

Gut Bacteria Crucial To Healthy Aging

Conclusion

The composition of the gut microbiome appears to determine whether we age gracefully or not and whether we get sick as we age or not. Everything depends on the diversity of the gut flora. There are bacteria in the gut that are good for us and also bacteria that are bad for us. Metformin has been shown to stimulate the good gut bacteria to multiply. Dr. Ezcurra is continuing her research into this. She clearly stated that it should be possible for us to age in a better way and maintain health and quality of life in old age without drugs or surgery.

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Jun
02
2018

Combatting Aging using Artificial Intelligence

I found an article dealing with combatting aging using artificial intelligence. It comes from the April 2018 edition of the Life Extension Magazine.  Both of those concepts sound intriguing: “combatting aging”. It would be nice, if this would be a possibility! And “artificial intelligence” (A.I.) sounds mysterious. LifeExtension researchers have partnered up with an A.I. group, called Insilico Medicine.

Why did Life Extension engage in this project? Many people have side effects with the drug metformin, which is an old diabetes drug. It turns out that metformin stimulates anti-aging genes that help to elongate telomeres and also activate genes that prolong lives otherwise. The thought was to find out how exactly metformin protects against age-related disorders. Once researchers located the genes, they may be able to find herbs that can do the same as drugs with less side effects. Often herbs are safer than drugs.

Background regarding metformin

The FDA accepted metformin (trade name Glucophage) as the first-line therapy for type 2 diabetics, particularly if they are overweight or obese.

Side effects include gastrointestinal irritation with vomiting, cramps, diarrhea and flatulence. Even though this drug is not new, research does not fully understand all metabolic effects of metformin.

Promise of metformin as an anti-aging drug

A trial in Great Britain found that metformin has an interesting anti-aging effect. Diabetics on metformin lived longer than a control group of patients without diabetes who were not on metformin. The diabetics lived 15% longer than the controls. Further experiments with human cells and animal experiments showed that metformin is able to stimulate the mitochondria without producing as many free radicals. Free radicals cause inflammation that leads to heart attacks, strokes, Alzheimer’s and cancer. The suggestion is that all of these diseases will be suppressed when the patient is on metformin.

Mimicking the effects of metformin with three herbs

The co-operative research between the Life Extension researchers and Insilico Medicine researchers concentrated on finding data that would replace the beneficial effects of metformin with three herbs stimulating the same life-prolonging targets in human cells. This is not a small task. The following three herbs in combination cover more than 78% of the actions of metformin.

Withaferin A (found in Ashwagandha)

Weight loss

Withaferin A is a component of the life-prolonging herb ashwagandha. This herb is in use in Ayurvedic medicine because of its ant-inflammatory action; it is also anti-diabetic, anti-cancer, anti-obesity and has appetite-regulating activities. An important observation by researchers was that within 21 days of exposing obese mice to withaferin A they lost 23% of their weight. Other mice on the same diet received control solutions and did not lose weight.

Effect on neurodegenerative disease

There is a neurodegenerative condition, called Lou Gehrig disease (=amyotrophic lateral sclerosis). A group of mice that were the subjects of genetic modification to develop Lou Gehrig disease received withaferin A in their food. Compared to controls without withaferin A they had a 39% reduction of damaged proteins in their spinal cords. They also had 60% less loss of motor nerve cells. These are the nerve cells that pass on the electrical signals between the brain, the spinal cord and into the muscles. The life span of these animals that received withaferin A was 5.4% longer than control animals.

Ginsenoside (found in Ginseng)

The structure of ginsenoside is steroid-like. As the name already suggests, it is present in ginseng. The Insilico Medicine team noticed that it affects many of the same age-decelerating pathways like metformin. Ginsenoside prevents damage to the DNA and prevents loss of mitochondria, particularly in the brain and heart. In cancer cases ginsenoside also suppresses cancer stem cells, which slows down cancer growth. All in all ginsenoside reduces inflammatory changes; it also fights neurodegenerative diseases, cardiovascular diseases and cancer.

Gamma linolenic acid (present in borage seed oil)

Gamma linolenic acid (GLA) is a fatty acid. The source of it is the evening primrose plant, black currant oil or borage. The Insilico Medicine researchers found that many pathways that metformin triggers are also responding to GLA. GLA can reduce inflammation, help with adaptation to stress can modulate metabolism and participates in regulation of gene expression. GLA is also part of energy sensing in diabetes and obesity. It also can slow down cancer development.

Discussion

One has to be cognizant of the fact that LifeExtension is in the business of selling herbal supplements. It would be in the company’s interest to find an herbal combination that mimics what Metformin does. They say they have found it; so we are told in the April 2018 article of the LifeExtension magazine. But a 78% overlap of actions when the herbs were compared to metformin is not a 100% overlap.

Conflict of interest

There seems to be a conflict of interest between doing basic research on anti-aging and marketing an anti-aging product. I like to see confirmation of these findings by other independent researchers. I am not too keen to spend $1.40 every day for the rest of my life in the hopes that this herbal concoction would slow down aging. Also to state that this mix of three herbs would do the same as Metformin is a large leap of faith. At this point I am not even ready to swallow metformin just because of one trial in England that showed a beneficial anti-aging effect.

Combatting Aging using Artificial Intelligence

Combatting Aging using Artificial Intelligence

Conclusion

The old dream of finding a pill for anti-aging is alive and well. If you believe this research you are likely to buy this pill and keep on taking it for the rest of your life. But I am not so certain that either swallowing metformin or swallowing this herbal concoction will do what the researchers were hoping for. They have done some basic research with mice and rats. But they tested each of the herbs  separately, and the researchers have then mixed the herbs and claim, that this mix will do what each single herb in isolation has done. We do not know anything about the interaction between these herbs. We do not know whether there will be the same anti-aging results with the mix. All these claims are yet subject to more testing.

Proposed clinical trial

I like to see a human trial where the anti-aging pill of Life Extension is given once per day for several years (let’s say 5 years). After that anti-inflammatory indicators, telomere length and toxicity should be tested in each subject that is part of the study. If trials like this were successful in humans, I would consider buying this new supplement, but not any earlier!

Oct
08
2016

Vitamin D3 Protects Your Brain

More and more studies are showing that vitamin D3 protects your brain. It protects against MS, but also against Parkinson’s disease and Alzheimer’s disease. In the following I will review what evidence there is to support each of these topics.

Vitamin D3 protects your brain from multiple sclerosis (MS)

It has been known for some time that in the northern hemisphere MS is more common because of the lack of sunshine, which in turn produces less vitamin D3 in the skin.

MS is an autoimmune disease where immune cells attack the lining of nerves. Both nerve cells and immune cells have vitamin D receptors. It appears that immune cells are calmed down by vitamin D3 and remission of an MS relapse is more likely.

There are two forms of MS, the relapsing-remitting MS and the progressive MS. The first one (relapsing-remitting) is more common. After a bout of active MS, the illness calms down and the condition of the patient is stable for some time until the next relapse occurs.

With progressive MS there are two forms, primary progressive MS and secondary progressive MS. The primary form is a case of MS where symptoms steadily worsen, without any remission. The secondary form of progressive MS occurs at the end of fairly stable relapsing-remitting MS. Symptoms become more pronounced and the condition deteriorates steadily from there.

Progression and disability in MS patients with various vitamin D3 levels

Dr. Fitzgerald and colleagues published a study in JAMA Neurology in 2015.

They took 1482 men and women who were on interferon beta-1b treatment. This treatment utilizes the immunomodulator interferon beta-1b and reduces the number of relapses in patients with MS. The study took place between November 2003 and June 2005. Results were analyzed between June 2013 and December 2014. The researchers measured vitamin D levels (as 25-hydroxy vitamin D). The vitamin D levels were obtained at baseline, at 6 months and 12 months.

The number of brain lesions were measured by MRI scans. All of the patients also underwent a functional test, called expanded disability status scale. This measured impairment of ambulation, ability to communicate and activity levels.

Results of this study showed marked differences between patients with high and low vitamin D levels. Those patients who had the highest vitamin D blood levels (more than 40 ng/mL) had the lowest rates of new MS lesions. Previous studies had found that a low blood level of vitamin D (less than 25 ng/mL) in patients was associated with a much higher risk of developing MS. Dr. Fitzgerald’s study showed that a 50.0-nmol/L increase in serum vitamin D levels associated with a 31% lower rate of new MS lesions. Patients with the highest vitamin D level of more than 100 nmol/L had the lowest amount of new MRI lesions (47% less than the patients with the lowest vitamin D levels).

Another study showed that a low-dose vitamin D level accelerated MS. There was a 5.9-fold risk converting the initial relapsing-remitting form of MS into the secondary progressive form of MS.

All these studies show that vitamin D3 can decrease the risk of getting MS. In addition vitamin D3 also delays progression in those who have MS.

Vitamin D3 protects your brain from Parkinson’s disease

Vitamin D3 plays a role in preventing Parkinson’s disease.

Parkinson’s disease is a neurodegenerative disease that causes tremor in muscles, causes balancing problems and eventually can lead to dementia. A metaanalysis was done in 2014 and 7 studies where identified to be relevant. The authors were looking for correlation of vitamin D levels with Parkinson’s disease. The study included 1008 patients in the metaanalysis with 4,536 controls.

  • Patients with a vitamin D level of less than 75 nmol/L had a 1.5-fold higher risk of developing Parkinson’s disease than the controls.
  • Patients with a vitamin D level of less than 50 nmol/L were at a 2.2-fold higher risk of developing Parkinson’s disease.

Another metaanalysis utilized 5,690 Parkinson’s disease patients and 21251 matched controls.

It found that vitamin D levels of less than 20 ng/ml were associated with a risk of 2.08-fold to develop Parkinson’s disease. Interestingly, vitamin D3 supplementation reduced the risk of Parkinson’s disease by 38%. Outdoor work reduced the risk of developing Parkinson’s disease by 28%.

Vitamin D3 protects your brain from Alzheimer’s disease

Alzheimer’s disease is a neurodegenerative disease of old age. We know that it is much more common in patients with type 2 diabetes where insulin levels are high. Studies have shown that Alzheimer’s disease can be termed type 3 diabetes.

The resulting neurofibrillary tangles and amyloid-beta deposits damage nerve cells, which are responsible for the memory loss and the profound personality changes in these patients.

What does vitamin D3 have to do with this?

A 2014 study showed that a low vitamin D level was associated with a high risk of dementia and Alzheimer’s disease.

Specifically, the researchers found the following observations.

  • Vitamin D level of less than 10 ng/ml: 122% increased risk of Alzheimer’s
  • Vitamin D level 10 to 20 ng/ml: 51% increased risk of Alzheimer’s

The same research group found in two trials that vitamin D deficiency leads to visual memory decline, but not to verbal memory decline.

Vitamin D3 combined with metformin suppresses cancer

The newest development with respect to vitamin D3 is the finding that it also has anti-cancer effects. Dr. Li demonstrated that vitamin D reduced prostate cancer cell line growth by 45% while metformin alone reduced it by 28%.

But when both vitamin D and metformin were present in the cell cultures there was growth inhibition of 86%. Dr. Li explained that vitamin D potentiated the growth inhibitory effect of metformin.

Vitamin D3 protects your brain: guidelines to proper vitamin D3 dosing

For years the medical profession stated that 400 IU of vitamin D3 would be enough supplementation. It may be enough to prevent rickets in children. But these low doses will be insufficient in many patients who are deficient for vitamin D to prevent MS, Parkinson’s disease, Alzheimer’s disease or cancer.

A study on medical staff in Northern India showed that 85% of the staff had very low vitamin D levels of less than 10 ng/ml.

It took high doses of vitamin D3 to increase the vitamin D level in the blood.

Generally supplements of vitamin D3 of 5000 IU to 8000 IU are the norm now. But some patients are poor absorbers and they may require 15,000 IU per day. The doctor can determine the patient’s requirement for vitamin D by doing repeat vitamin D blood levels (as 25-hydroxy vitamin D). The goal is to reach a level of 50-80 ng/ml. The optimal level with regard to nmol/L is 80 to 200 (according to Rocky Mountain Analytical, Calgary, AB, Canada).

Vitamin D3 Protects Your Brain

Vitamin D3 Protects Your Brain

Conclusion

Many people are deficient with regard to vitamin D, and they do not know it. The most important thing is to do a vitamin D blood test to assess your vitamin D status.

We know for a long time that vitamin D plays a role in bone metabolism and this is why women approaching menopause often need vitamin D3 supplementation. But it may come to you as news that vitamin D3 also protects from MS, Parkinson’s disease and Alzheimer’s disease. In addition, as indicated above, we know that vitamin D3 when taken regularly suppresses many cancers.

When you realize that all body cells have vitamin D receptors on their surface, it is no surprise that vitamin D3 is so important to take. The vitamin D3 receptors must be there for a reason. When you deprive your body of this valuable vitamin, the high risk of degenerative diseases will be the consequence.

Feb
08
2014

Sugar As A Cause Of Cancer

It has been known for a long time that cancer cells can survive without the ordinary aerobic pathways of energy production. They can get energy from a metabolic pathway, which bypasses normal cell metabolism (aerobic glycolysis). But many attempts of designing a cancer therapy to exploit this difference have so far been unsuccessful.

This Mayo Clinic website even explains that it would be a myth that cancer would grow better with sugar. The following pieces of research question this myth.

Sugar makes cancer grow faster (activates oncogenes) in fruit flies

In this study from the Icahn School of Medicine at Mount Sinai in New York City fruit flies were used as an animal model. You may ask, why fruit flies; we are not fruit flies, we are humans! As incredible as it sounds, on a cellular level our cell metabolism and the cell metabolism of fruit flies is identical. But the generation time of fruit flies is much shorter and results can be seen in days and weeks. To achieve the same in human trials would take months and years. Also, researchers could breed a strain of fruit flies that was susceptible to develop tumors. When they were fed sugar, the fruit flies developed insulin resistance within a short time. This model was chosen by the researchers as it is known for some time that in humans insulin resistance from diabetes, obesity, and other metabolic diseases leads to a higher risk of developing breast cancer, liver cancer, colon cancer and pancreatic cancer. The researchers wanted to sort out what the metabolic advantage of the cancer cells was under these conditions.

The researchers found that the sugar in the diet activated silent cancer causing genes (called “oncogenes)” in the fruit flies that in turn helped to promote insulin resistance and the development of tumors. Because of the insulin resistance sugar could not enter into the normal body cells, but the tumor was using up all of the sugar allowing the tumor cells to multiply at a rapid rate. The end result was that the sugar from the diet fed the cancer cells directly making them grow faster. Interestingly, when these flies that had developed tumors on a high sugar diet were switched to a high protein/low sugar diet, the tumors stopped growing and were contained.

In this fruit fly example the researchers were subsequently able to block cancer cell growth by special cancer suppressing drugs (acarbose, pyrvinium and an experimental drug AD81), which were given in combination. 90% of the flies given the triple-drug treatment survived to adulthood while control flies not treated with this regimen all died of their tumors.

Although this model was only done in fruit flies and one could question whether or not this was relevant to what is happening in human cancer patients, the following piece of research puts this fear to rest.

Sugar As A Cause Of Cancer

Sugar As A Cause Of Cancer

Human breast cancer cell study in vitro

In January 2014 the American Society for Clinical Investigation published a collaborative study between the Lawrence Berkeley National Laboratory, Berkeley, California, CA and the Hokkaido University Graduate School of Medicine, Japan, which used human breast cells in tissue culture showing that sugar could cause breast cancer.

The original papers of this US/Japanese research team are quite technical and I do not expect you to understand this link where it is published. I posted it for those who want in depth information. The researchers used a simple tissue culture model where they could observe tumor growth in cell cultures under the microscope using a gel where the breast tissue samples were placed side by side with normal breast cells that served as controls. The cell cultures of both normal cells and malignant cells were obtained from the same reduction mammoplasty tissue samples. This way the cell cultures mimicked a situation as close to the reality of what is going on in a woman’s body when breast cancer develops.

The normal breast epithelial cells were seen in culture to get organized as a roundish cell formation (an acinus formation) while the cancer cells were growing as irregular cell clumps. This visual effect was reproducible and is depicted in the paper. With high sugar concentrations in the growth medium breast cancer cells multiplied at a faster rate, not so the normal cells. But some normal cells underwent a transformation into abnormal and cancerous cell types. On the other hand, when sugar concentrations were severely restricted, morphological changes took place where cancer cells slowed down their growth or stagnated while some of them even changed into the normal cell formation (acinus formation). Using various known oncogene stabilizers the investigators could show that the same effect was noted as with the low sugar concentration in the growth medium.

The investigators tested whether other cell lines of breast cancer would show similar results as to the effects of sugar feeding or restriction. They were able to show that high sugar feeding activated cancer cells, no matter where the cancer cell lines originated. The authors discussed that metformin, which is known to control the metabolism in diabetic patients and lowers blood sugar levels, has also been shown to calm down growth of cancer (due to stopping oncogene stimulation), which improves the survival rates of many different cancer types in diabetic patients; it also reduces the risk of developing cancer in those who are taking metformin.

Other investigators have shown in mouse experiments that an impressive lowering of cancer rates could be achieved with low carb diets.

Human evidence for cancer causation and cancer prevention

Several clinical studies seem to indicate that there is a higher cancer rate in diabetics where insulin resistance can lead to activation of cancer producing genes (called oncogenes) and cause various cancers. In this link colorectal cancer and pancreatic cancer are discussed in relationship to diabetes and insulin resistance. High glycemic foods (sugar, starchy foods) were associated with breast cancer, colorectal cancer and endometrial cancer. The majority of trials showed this association although not all. The more obese patients were, the more pronounced the insulin resistance was and the more the relationship to these cancers became apparent. A diet that is high in starchy foods like potatoes, rice and bread is causing pancreatic cancer as was shown by researchers at the Dana-Faber Cancer Institute, Brigham and Women’s Hospital and Harvard School of Public Health. High glycemic diets have shown to cause colorectal cancer, diabetes and being overweight. The Standard North American Diet (SAD) is a pathway to many chronic illnesses due its high load in refined carbohydrates. Ironically the abbreviation for it is “SAD”, which in my opinion reflects adequately its sad influence on health and well being. We know now that sugar and starchy foods lead to insulin overproduction, which in turn causes the metabolic syndrome (also known as “insulin resistance”). This causes the immune system to weaken and fat to be deposited as visceral fat in the stomach area. Visceral fat is metabolically very active as it secretes cytokines like tumor necrosis factor alpha (TNF alpha), COX-2 enzymes and others. Insulin and growth factors from the visceral fat gang up together with the elevated blood sugar, which activates tumor-producing genes (oncogenes) to cause cancer.

While cancer rates are higher in patients with insulin resistance, they were lower in patients who did have normal insulin levels. It is important to concentrate your efforts on normalizing weight, which will normalize insulin sensibility and avoid the development of cancer. Sugar avoidance and avoidance of cereals and starchy foods will help you achieve this goal.

Conclusion

Although the idea that sugar could cause cancer has been around since 1924 (Dr. Warburg), it has taken up to now to be proven in animals and humans.

The purpose of this blog was to show how there is a connection between the consumption of sugar and starchy foods and various cancers in man. Animal experiments are useful in suggesting these connections, but many clinical trials including the Women’s Health Initiative have shown that these findings are also true in humans. It is insulin resistance due to sugar and starch overconsumption that is causing cancer.

We are now in a position to know why people who consume a low carb diet, develop less cancer than people who consume a high carb diet. I have followed such a low carb diet (also known as low-glycemic index food diet) since 2001 and find it easy to follow. However, I do not dispute that it takes some discipline to change the old way of eating to the new one. The benefits are definitely worth it: you are feeling well now and you are staying well as you age.

More information about hyperinsulinism that can cause breast cancer: http://nethealthbook.com/cancer-overview/breast-cancer/causes-breast-cancer/

Last edited Nov. 7, 2014

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Nov
09
2013

Successful Diabetes Treatment Requires Patient’s Discipline

90% of all diabetes cases are due to type 2 diabetes, which is associated with being overweight or obese. The other 10% are due to type 1 diabetes, which is caused by an autoimmune disease within the pancreas destroying the insulin producing beta cells. Diabetes, type 1 often occurs in childhood (hence the name “juvenile diabetes”), while type 2 diabetes is a condition of the middle aged and older population. There is however an alarming trend: overweight or obese youngsters are also being diagnosed with type 2 diabetes. Here I am discussing type 2 diabetes.

Causes that trigger diabetes

There is not just one way to get diabetes; it usually is a multifactorial disease. Sure, genetics play a minor role. But you need to have epigenetic factors to trigger the genes to develop diabetes: eating too much sugar, eating wheat and wheat products, drinking soda drinks that contain sugar or high fructose corn syrup. Alcohol binges can also cause diabetes as can accumulation of excessive weight (a body mass index above 25.0). Even when there is no genetic risk in your family (your family tree has nobody that came down with diabetes and all your ancestors lived into their 90’s), you can still develop diabetes, if you are exposed to one or more of the risk factors mentioned.

What is the reason why diabetes occurs?

At a Keystone Symposium from Jan. 27 to Feb.1, 2013 in Keystone, Colorado (Ref.1) leading scientific researchers gathered to discuss exactly this question. There seem to be several mechanisms, all of which lead to diabetes. It has been known for some time that in type 2 diabetes insulin resistance develops that renders the cells incapable of absorbing blood sugar (glucose) from the blood into the cells. It is because of this insulin resistance that doctors can diagnose diabetes when blood sugar levels are high.

Successful Diabetes Treatment Requires Patient’s Discipline

Successful Diabetes Treatment Requires Patient’s Discipline

There are at least 5 mechanisms that are presently known that can cause insulin resistance (and thus diabetes) by itself or in combination. For a deeper understanding of diabetes it is crucial to be aware of these. Without knowing the enemy, you cannot fight it.

1. When a person eats too much sugar or fructose the liver converts this into excessive fat that is accumulated in the body’s cells. As a result insulin receptors are becoming inefficient in absorbing sugar from the blood, and blood sugar levels stay high. The pancreas reacts to this by making even more insulin, which after a few years will cause the pancreas to fail in producing insulin. At this point the patient requires insulin or else gets into a diabetic coma.

2. Chronic inflammation is another mechanism that has been shown to cause insulin resistance. Obesity, the metabolic syndrome and diabetes have a common inflammatory denominator that results in insulin resistance. With the aging process there is also deterioration of mitochondrial function (mitochondria are the mini batteries inside of every cell that are responsible for you having energy). This causes fat accumulation and also insulin resistance. Exercise and weight loss are effective in combatting insulin resistance. Fasting has also been shown to improve insulin sensitivity.

3. The metabolism of visceral fat (the type of fat causing the apple appearance in obesity) is highly active and is associated with an increased risk for heart attacks and developing diabetes. The pear shaped woman runs less of a risk, as the fat around the hips is not metabolically active. On the other hand when these women enter into menopause, they also develop abdominal fat (apple-like fat distribution) with a high secretion of inflammatory substances causing insulin resistance, heart attacks and strokes.

4. Another mechanism of causing inflammation comes from invasion of organs with fat cells. The development of fat toxicity from these displaced fat cells can also cause insulin resistance. Heart cells have been shown to die from fat toxicity and in the pancreas the insulin-producing cells can be killed by fat toxicity as well causing diabetes or making existing diabetes worse.

5. Interestingly another line of research, namely researching binge drinking, has revealed that there is a short-term insulin resistance that lasts for several days until the alcohol has been properly metabolized. It is of concern that adolescents who are experimenting with binge drinking are very vulnerable to develop brain damage from this habit.

Consequences of insulin resistance

We know that insulin resistance is the cause for adult onset, type 2 diabetes. It is entirely preventable. But there are powerful influences on people’s lives that will allow one or more of these factors mentioned to cause diabetes. The most common cause is putting on excessive weight. The reason for this is that people like to eat fast foods, drink sugar-containing sodas, and feast on processed foods, bagels and cookies. The end result is a change of the metabolism with an increase in triglycerides from the liver, an increase in LDL cholesterol, particularly the very low-density lipoprotein sub fractions of cholesterol. It has been known for some time that this is the connection to the high, premature death rates from heart attacks in diabetics, in people with obesity and in people with the metabolic syndrome. Hardening of the arteries is accelerated by the deposition of foam cells in the walls of arteries. These are scavenger cells (macrophages) that have engulfed noxious fats. This leads to narrowed coronary arteries and also a general narrowing of arteries all over the body including the brain vessels. In diabetics hardening of the arteries is accelerated and leads to premature strokes, heart attacks and heart failure, kidney failure, blindness and amputations of limbs.

Important tests for borderline diabetics

I you have a fasting blood sugar that is above 100 mg/dL (5.5 mmol), but less than 126 mg/dL (7 mmol) you are considered to be prediabetic or “borderline diabetic”. In this case rather than waiting for disasters in terms of cardiovascular disease, take action and ask your doctor to do the following three tests.

a) Arrange for a glucose tolerance test where you are given 75 grams of glucose; then blood tests are taken at one, two and three hours after this challenge dose. These blood tests are checked for blood glucose levels and insulin levels and tell the doctor exactly what is going on in terms of your sugar metabolism. It shows the glucose clearance and also the insulin response from your pancreas.

b) Have a hemoglobin A1c test done: it shows how your blood sugars have been controlled over the last 2 to 3 months.

c) You also need a VAP (vertical auto profile) test, which tests your lipid profile. Both prediabetics and overtly diabetics have been shown to have lipid profile disorders. Apart from low values in sub fractions of HDL cholesterol this test will also measure the very-low density lipoproteins (VLDL), which has been shown to be responsible for heart attacks and strokes.

With these three tests your doctor can  tell you more accurately what treatment protocol you require to succeed in controlling or curing your pre diabetes or diabetes.

Conventional treatment of diabetes

The conventional treatment of diabetes is to send the patient to a dietician, to ask the patient to do regular exercises and to either start them on hypoglycemic drugs or on insulin injections. Unfortunately the dietician often will encourage the patient to eat “healthy multigrain bread”, which will stimulate your taste buds to eat more sugar, high fructose corn syrup and starchy foods making weight loss impossible. Often the treating physician is satisfied that a hemoglobin A1c of 7% or less is good enough for the diabetic. But non-diabetic people have a hemoglobin A1c of 4% and 5.6%. This should be your goal or you will suffer the consequences of uncontrolled diabetes.

This is what I would call the conventional, symptomatic treatment approach. This may be the approach for patients who are not willing to seriously change their lifestyles, but it is more powerful on the long-term to treat diabetes by treating the underlying causes.

Alternative treatment approach for diabetes

Based on the above discussion regarding the various causes of insulin resistance, it is important to analyze what would be the main contributory factors in your particular case of diabetes.

Here are some suggestions:

1. If you are on the typical North American diet, also known as Western diet, it would be important to face the fact that wheat, wheat products in processed foods and sugar including high fructose corn syrup are the main culprits in stimulating your appetite and making you a sugar and wheat addict. Ref. 2 describes this in detail and offers 150 recipes to overcome this addiction. For more information just follow this reference text. Essentially it is a wheat-free Mediterranean type diet without rice, pasta and bread. You will shed significant amounts of pounds within a short period of time and feel a lot more energetic (due to revitalization of your mitochondria). At the same time insulin resistance is disappearing, because the insulin receptors are fully functional again. The insulin production of the pancreas will go down to normal levels and fat from the visceral fat storage gets melted away resulting in less inflammatory substances circulating in your blood.

2. A regular exercise program in a gym with an aerobic component (30 minutes of treadmill for instance and 20 to 30 minutes of isometric machine exercises) will help you to lower the triglycerides, and increase the healthy HDL cholesterol. It will also improve insulin sensitivity and control inflammation in your body. The best is to exercise 7 days per week. Remember your body works for you 7/7 every week, but for those of you who need a little rest in between 5 days per week is still very good. You may have to adjust your medication and insulin dose downwards, ask your physician about that.

3. Cut out alcohol. This may sound radical to you, but studies show this to be true. I have not mentioned cutting out smoking (it is causing inflammation and insulin resistance), because this is an absolute must that is given. When it comes to alcohol, the famous 1 drink per day for cardio protective purposes may not show up statistically as a bad effect, but your body will nevertheless get the message and let you age somewhat faster than a person who stays sober all the time. Staying sober will allow your brain to think clearly and adhere to your overall lifestyle approach in treating diabetes. Cutting out alcohol protects your brain (including the hypothalamus), liver and pancreas and prevents the prolonged periods of insulin resistance mentioned above that last for days. By keeping your hypothalamus in good working order, your hormone balance will stay stable for as long as possible until you reach menopause (for women) or andropause (for men). When you reached this milestone, I suggest you engage in bioidentical hormone replacement, which I have reviewed here. Hormones are essential to keep you younger for longer.

4. It is useful to monitor your blood sugar with a home glucometer, as this will show you when your blood sugar normalizes. Stay in touch with your doctor at all times, as this will help you in your overall management of your diabetes. Also, you will want to discuss with your doctor that you should have a blood tests called “hemoglobin A1c” measured every three months to see how well your diabetes is controlled. It should be below 7% for sure, but better below 6%. Non-diabetic people have levels of 4% and 5.6%. You may not know that hemoglobin A1c is actually measuring the amount of advanced glycation end products (“AGE”) of red blood cells. These AGE substances essentially are firmly bound sugar/protein compounds that shut down the cell metabolism wherever they are formed. In my opinion it is best to aim at a hemoglobin A1c level of non-diabetic people (4% and 5.6%) to avoid the consequences of tissue damage of all vital organs, which is the reason why long-term diabetics have a life expectancy of 15 to 20 years shorter than non-diabetic persons. Some diabetic patients may benefit from the oral hypoglycemic drug, metformin (brand name: Glucophage), which has anti-inflammatory properties and is used in patients with type 2 diabetes and a high fasting insulin level, but this is a decision requiring your physician’s input.

5. Supplements: There are some supplements that are useful to take as an adjunct, like chromium, which helps insulin to transport glucose into the cell; alpha-lipoic acid, an antioxidant, which is useful to prevent glycation (formation of a complex between sugar and protein, which prevents normal cell functioning); and coenzyme-Q10, which supports your heart (A4M recommends 400 mg per day, higher than Dr. Weil’s link). Other supplements of merit are curcumin, cinnamon, genistein and silymarin (standardized extract of milk thistle), which suppresses a pro inflammatory molecule, which in turn helps to fight insulin resistance (Ref. 1). Omega-3 fatty acid supplements are anti-inflammatory and will improve insulin resistance as well (dosage 1000mg or more per day). According to Ref. 3 vitamin D3 is useful as a supplement for diabetics, because it activates DNA, is involved in cellular repair and deficiency of it is known to lead to higher mortality rates in diabetics. Ref. 3 recommends between 1000 and 4000 IU of vitamin D3 daily and suggests doing blood tests to measure effective vitamin D3 levels (keep 25-OHD in the blood between 30 and 80 ng/mL).

6.Patients whose pancreas no longer produces insulin will need insulin injections, but instead of using long-acting insulin once per day the best results in getting blood sugar control is by injecting insulin three or more times per day using short acting insulin. It is important to always monitor the blood sugar lowering effect by glucometer readings; the injections are best given just before meals (recombinant human insulin is the preferred insulin to be used). Ask your physician or diabetic coach for more details.

Conclusion

Diabetes used to be a dreadful disease that caused premature heart attacks, strokes, blindness, kidney failure, and limb amputations. With aggressive management of diabetes as well as strict lifestyle intervention this has changed. A diabetic who treats the causes of the illness can have a normal life expectancy. In many cases the initial diagnosis of type 2 diabetes can disappear, when treatment was started early enough and insulin resistance could be stopped in its tracks. Without the patient’s full co-operation disciplining him/herself to follow through on all of these recommendations the caregiver will fail in controlling the patient’s diabetes. It is the patient who owns the problem; it is the patient who needs to make every possible effort and follow through on all of the details of dieting, exercising, blood sugar monitoring using a glucometer and taking the required supplements.

More information on diabetes: http://nethealthbook.com/hormones/diabetes/type-2-diabetes/

Reference

1. http://www.lef.org/magazine/mag2013/oct2013_2013-Keystone-Diabetes-Symposium_01.htm

2. William Davis, MD: “Wheat Belly Cookbook. 150 Recipes to Help You Lose the Wheat, Lose the Weight, and Find Your Path Back to Health”. HarperCollins Publishers LTD., Toronto, Canada, 2012.

3. Rakel: Integrative Medicine, 3rd ed. © 2012 Saunders. Integrative Therapy; Supplements.

Last edited Dec. 17, 2014

Nov
01
2008

Pills For Diabetes Not Always Useful

Oral anti-diabetic drugs have been on the market for decades. They are often prescribed to patients with type 2 diabetes in an effort to control blood sugar levels. Type 1 diabetes patients, those who suffer from diabetes since childhood, generally require a different therapeutic approach. They receive insulin in the form of injections, or more recently by pump. The usefulness of the oral antidiabetic drugs has been researched by Elizabeth Sevin, PhD,MPH of John Hopkins Blomberg School of Public Health, Baltimore. Pooled data analysis found that patients who took one of the older medications, metformin, were at a reduced risk of death from cardiovascular illness. Metformin works by blocking the breakdown of glycogen (a storage form of sugar) in the liver, reduces absorption of sugar from the gut and increases insulin sensitivity thus controlling blood sugar more tightly. This protected the heart from cardiovascular illness. None of the other oral medications for type 2 diabetes was significantly linked to cardiovascular illness, but cardiovascular disease and mortality was higher in the patient group that took the drug rosiglitazone.

Pills For Diabetes Not Always Useful

How metformin works for type 2 diabetes

Due to the controversial reports about this drug, the researchers took a closer look at all the other oral anti-diabetic medications. None of them, not even the newest ones, proved to be superior, and the only one that showed a slight benefit was metformin. The author cautions that the association is too weak to be of significance, and a lot more long-term research would be needed to substantiate the benefits for cardiovascular protection.

More information on Diabetes: http://nethealthbook.com/hormones/diabetes/type-2-diabetes/

Comments on Nov. 18, 2012: I do not see any further benefit for more research on oral anti-diabetic agents. Rather this type of research would indicate that subcutaneous insulin treatment 3 or 4 times per day as originally suggested by Banting and Best is still the best treatment for diabetes coupled with an exercise program and a low fat, low glycemic carbohydrate diet.

Arch Intern Med. 2008;168:2070-2080

Last updated Nov. 6, 2014

Jul
01
2008

High-protein, Low-refined carb diet useful in controlling diabetes

Diabetes type 2 is often associated with obesity (body mass index higher than 30.0 kg per meter squared). At the 16th European Congress on Obesity in Geneva Dr. Neil Mann presented a study of 99 patients. Half were put on a high protein diet, the other half on a high carbohydrate low glycemic index diet and followed for one year with periodic blood tests and examinations by their family doctors. The study population’s age ranged from 30 to 75 years and their body mass index varied from 27 to 40. The hemoglobin A1C level that is a measure of severity of the diabetic condition ranged from 6.5% to 10%.

The high-protein diet was structured so that 30% of calories came from protein, 40% came from carbohydrates and 30% came from fat. With the high-carbohydrate low glycemic index diet 15% of the calories came from protein, 55% from low glycemic index carbs and 30% from fat. In both groups the total calorie intake per day was restricted to 1500 calories and the carbohydrates were given as low glycemic index carbohydrates (less processed). In both groups the diabetes was better controlled with hemoglobin A1C, triglyceride levels and cholesterol levels normalizing. Both groups also showed an equal amount of weight loss that stayed down as long the patients adhered to the diet. However, the high-protein group was able to reduce diabetes pills (metformin) and insulin achieving the same results as the high-carbohydrate low glycemic index group that could not reduce their medications. The conventional approach is to use a low-fat, high-carbohydrate diet along with medication. However, this diet tends to lead to higher triglyceride levels, higher blood sugar levels and a reduction in the good cholesterol (HDL).

High-protein, Low-refined carb diet useful in controlling diabetes

High-protein, Low-refined carb diet useful in controlling diabetes

Dr. Mann who is a professor and head of the department of nutrition and food science at RMIT University, Melbourne, explained the people get confused when they hear the term high-protein diet as they think of the Atkins diet where the protein component was much higher. The diet that was investigated here is a more natural diet consisting of slightly higher protein and less processed carbohydrates. By containing more fat than in the conventional diabetic diet the patient is not getting hungry and finds it easy to stick to the diet, which leads to weight loss and improvement of the metabolism. Many patients can normalize their blood values and often even get off their diabetic medication (under careful supervision by their treating physician). The physician will address the three components of diabetic control (energy balance, glycemic control, and vascular complications) by recommending to the patient this high-protein/low-carb diet. This likely will replace the conventional approach of using a low-fat, high-carbohydrate diet.

More information about a Mediterranean type diet in firefighter’s, which is very similar to this study: http://nethealthbook.com/news/mediterranean-diet-benefits-us-workers/

Reference: 16th European Congress on Obesity, Geneva June 23, 2008

Last edited November 4, 2014

Apr
01
2005

One Shot For Better Blood Sugar Control

People with permanent health conditions face the need for lifelong medications, and patients with type 2 diabetes see insulin shots as part of an everyday routine. There are different types of insulin, which helps in tailoring the medication to the needs of the patient.
It is old news that a new type of insulin under the name insulin glargin can be used for the treatment of type 1 diabetes. The news of a study just published in February is, that also patients with type 2 diabetes benefit from insulin glargin. Often the standard treatment with diabetes drugs does not provide optimal control of blood sugar levels.
371 type 2 diabetes patients with inadequate diabetes control who were not supplemented with insulin were part of a 24-week clinical trial in Bremen, Germany, headed by Dr. Hans U. Janka.

The patients received an antidiabetic combo consisting of sulfonylurea and metformin. These patients were randomly picked, and they received a morning dose of glargine insulin injection along with the antidiabetic medication. Others did not receive the oral medication, but were administered twice-daily injections of NPH insulin. Patients were monitored for the level of glycosylated hemoglobin (= HbA1c), which is the best indicator for diabetes control. The improvements in laboratory tests were more pronounced in the group that received the combination between an oral antidiabetic and glargine injection. In addition 46% reached HbA1c levels of 7% or less, which is excellent long-term blood sugar control, as compared to only 29% of the NPH insulin group. Fasting blood sugar levels also showed improvement. There is a risk of patients becoming hypoglycemic. Again, the risk was significantly lower in those who were on the glargin combination, than those who were on the NPH insulin.

One Shot For Better Blood Sugar Control

One Shot For Better Blood Sugar Control

These results show that one single injection, which is added to the oral medication, can help type 2 diabetes patients, whose condition has been poorly controlled. Glargine insulin has been approved in Canada already in 2002, but due to supply problems it is only now expected to be on the pharmacy shelves soon.

More information on treatment of diabetes with insulin: http://nethealthbook.com/hormones/diabetes/treatment-diabetes-insulin/

Reference: National Review Of Medicine, March 15,2005,page22

Last edited October 28, 2014