Oct
14
2017

A New Genetic Marker For Alzheimer’s

“A new genetic marker for Alzheimer’s”; so reported a study dated August 11, 2017. Most of all, they found that a genetic marker, TOMM40 was stronger than the established genetic marker APOE4. It seems like the older studies overlooked the importance of the new TOMM40 genetic marker. This new marker may have been present at the same time as APOE4.

Details of study regarding a new genetic marker for Alzheimer’s

The APOE4 is especially relevant for the formation of lipoproteins. APOE4 showed a strong association with the formation of amyloid plaque. This is located in the brain areas where Alzheimer’s disease developed. Therefore the thinking in the past was that APOE4 would be the culprit behind memory loss and Alzheimer’s disease. In contrast, the new study shows evidence that the TOMM40 genetic marker is the gene that actually orchestrates the development of Alzheimer’s disease. Thalida Em Arpawong is a postdoctoral fellow at the University of Southern California (USC) Dornsife College. She conducted research about the TOMM40 marker. Her supervisor was senior investigator Carol A. Prescott, who is a professor of psychology at the USC Dornsife College. She co-published the paper.

More info about the study involving a new genetic marker for Alzheimer’s

Professor Prescott used two verbal memory test results. They were the United States Health and Retirement Survey (HRS) and the English Longitudinal Study of Ageing (ELSA). In these tests immediate recall was compared to delayed recall 5 minutes later. Alzheimer’s patients have problems with short term memory recall.  In total the study examined 20,650 HRS participants and 11,391 ELSA participants. Their age was 50 years and above since this is the typical age for the onset of Alzheimer’s disease. Genetic data was part of the examination in 7,486 HRS participants and 6,898 ELSA participants. The scientists looked at 1.2 million genetic variations of the human genome to fit the memory loss. In conclusion, only one gene area, TOMM40 showed a strong association with decline in immediate and delayed memory recall.

Hence professor Carol A. Prescott summarized the findings: “The results from this study…raise the question of how many findings in other studies show an association with APOE4 that may in fact be due to TOMM40 or a combination of TOMM40 and APOE4.”

Possible future clues from a trial using TOMM40 marker

A review paper points out the start of a new trial, called TOMMOROW. The review paper points out that the location of APOE and TOMM40 are on chromosome 19 in very close proximity. Pioglitazone is a drug that controls diabetes. Patients tolerate it well. It is used in the TOMMORROW trial. As this review paper states the TOMM40 gene is responsible for the outer mitochondrion membrane. Consequently the paper states: the “outer mitochondrial membrane channel through which peptides and proteins travel into mitochondria to support mitochondrial function and biogenesis” is the key for understanding Alzheimer’s disease. Because pioglitazone is a drug that induces mitochondrial doubling the researchers hope that it will help Alzheimer’s patients.  It will probably be interesting to follow the phase 3 trial TOMMORROW, where research will observe the delay in onset of minimal cognitive impairment.

A New Genetic Marker For Alzheimer’s

A New Genetic Marker For Alzheimer’s

Conclusion

Research has found a new genetic marker for Alzheimer’s, TOMM40 that identifies a higher risk of getting Alzheimer’s disease. Its location is close to the marker APOE on chromosome 19. It appears that TOMM40 may be more reliable in identifying patients at risk for Alzheimer’s disease than the older APOE marker. As a result research has started a new phase 3 trial, called TOMMORROW. This will tell whether or not Pioglitazone, a diabetic drug maybe useful in delaying Alzheimer’s disease in high-risk patients.

Sep
09
2017

Young Heart Stem Cells Can Cure Old Hearts

Young heart stem cells can cure old hearts in rats. This is what research at the Cedars-Sinai Heart Institute in Los Angeles found. You may not be that impressed, because this talks about rats and not humans. But this is a brand-new concept, so of course research of animal experiments is first.

The heart experiment

Dr. Eduardo Marbán, MD, PhD, is the research director of the Cedars-Sinai Heart Institute. His idea was to take cardiac stem cells (called cardiosphere-derived cells) from hearts of newborn rats. He injected them into 22 months old rats. The human equivalent for 22 months old rats are older people with older hearts. Within one months of the stem cells’ injections the older rats had normal functioning hearts. Their telomeres were also normal. Telomeres are the caps of the chromosomes of the heart cells. The researchers were astonished to find that the previously short telomeres had become longer. This happened within only one month of the stem cell injections. To Marbán’s surprise the older rats also grew hair faster and gained 20% of their previous exercise tolerance limit. In other words, the injection of heart stem cells had rejuvenated the old rats.

Dr. Marbán has previously shown that exosomes play an important role with stem cell regeneration of old heart cells. These particles from the stem cell donor contain RNA and other growth factors.

Overview of how stem cells can reverse heart failure

Cardiovascular disease includes high blood pressure, coronary artery disease, stroke and congestive heart failure. About 2600 Americans die from cardiovascular disease each day in the US. This is roughly one death every 34 seconds. With old age, if a heart attack does not kill you, congestive heart failure will. With heart failure your heart ceases to pump enough blood through your system. Nutrients and oxygen need to reach all of our cells or it means death for the patient. With the knowledge of this serious background, stem cells have come into the focus in an attempt to combat congestive heart failure.

Animal experiments with stem cells in mice, rats and pigs have shown some progress in restoring better heart function. Researchers used different sources of stem cells, like cardiac stem cells that reside in the heart muscle itself. They also used other stem cell sources. Among these were myoblasts (from muscle), mesenchymal stem cells (from fat tissue) and bone marrow stem cells. Several smaller human trials showed that improvement of heart function was possible following a heart attack. In the procedure the surgeon opened coronary arteries and injected stem cells into the affected damaged heart muscle. How can we assess the result of a successful stem cell treatment? By measuring the left ventricular ejection fraction. This means that the heart can deliver a larger volume of blood every minute. The heart pumps more blood from the left ventricle with each heartbeat than before the treatment.

Other experiments that rejuvenate tissues of older animals

Another line of experiments in this paper shows that certain growth factors are necessary to activate stem cells.

  1. One experiment from the 1950’s describes the stitching together of the skin on their flanks joined an old and a young rat. After this procedure the blood vessels grew and joined the two animals circulatory systems. The older animals knee cartilage damage was no longer there, as the cells from the young animals’ blood had healed the damage.
  2. Research had no knowledge of this fact at that time. But another research group in the 2000’s repeated the experiment and could prove that the stem cells of the young animals activated the growth factors in the old animals.
  3. In 2004 Dr. Rando noted that muscle cells of aging mice were aging because of a lack of stimulation of the local skeletal muscle stem cells. These are satellite cells. Experiments similar to the rat experiment showed that there were factors in the blood of young mice that could re-activate stem cells in the muscles of old mice. Agility and movement of the older mice improved. The improvement in the older mice with knee arthritis disappearing and liver cells rejuvenating was astounding.

More evidence that rejuvenation of heart cells is possible

  1. Amy J. Wagers, a former colleague of Dr. Rando carried on experiments with respect to rejuvenation of hearts in mice. She and her colleagues found what stimulated the hearts of old mice. It was a protein called GDF11 (from young mice).  This 2016 publication describes the action of GDF11.
  2. A 2014 paper describes that GDF11 was able to restore aging muscles to a youthful state. But the researchers were also able to rejuvenate stem cell function in general with GDF11.
  3. Another paper describes that blood from young mice stimulates the brain of older animals to achieve rejuvenation. It is the protein of the young stem cells (called GDF11) and possibly other growth factors to bring about this rejuvenation. It works not only on heart cells, but also on hippocampus tissue in dementia models. This may be important in humans for treatment of Alzheimer’s disease.

“We can turn back the clock instead of slowing the clock down.” Dr. Toren Finkel said. He is the director of the Center for Molecular Medicine at the National Heart, Lung and Blood Institute. He went on to say: “That’s a nice thought, if it pans out.” But others who caution that overstimulation of stem cells could cause cancers say: “It is quite possible that it will dramatically increase the incidence of cancer,” Dr. Irina M. Conboy said, a professor of bioengineering at the University of California, Berkeley. “You have to be careful about overselling it.”

Degenerative changes in humans responding to stem cells

Many degenerative changes in humans respond to stem cell treatments. Are there stem cells present in degenerative tissue in humans similar to the animal experiments described above? Are the stem cells merely providing growth factors so the dormant stem cells jump into action and regenerate? Could it be that in future therapists could give a certain growth factor mix  intravenously to a patient, and the same effect as stem cell injections would be posssible? These are all unanswered questions, but research in the next decade should answer at least some of those questions.

Growth hormone improving heart function in heart failure patients

In 2008 a metaanalysis of human studies of congestive heart failure and treatment with human growth hormone (HGH) injections was a research topic. It showed an average increase of the ejection fraction by 4.3%. There were also increased cardiac output, decreased systemic vascular resistance and improved hemodynamic effects. The question is whether the effect is a direct effect on the heart muscle cells by HGH or whether HGH was recruiting dormant heart muscle stem cells. This is not clear at this point.

Young Heart Stem Cells Can Cure Old Hearts

Young Heart Stem Cells Can Cure Old Hearts

Conclusion

We have entered an exciting period of medical research. Although there is only a record of many animal experiments, there is overwhelming evidence that the same principles are true in humans. Many stem cell protocols for humans have already seen use for various applications. But stem cell treatments for heart disease are still in their early stages. As it becomes obvious from my review of this topic, some patients who were part of clinical trials have already experienced positive results. Congestive heart failure or poor pump performance following a heart attack have improved following various stem cell procedures. In the next few years there likely will be a proliferation of treatment options for patients. Although some critics have pointed out a possibility of cancer developing as a side effect of stem cell treatment, no evidence is noticeable at this point.

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Sep
02
2017

Resveratrol Effective In Humans

Resveratrol has been labeled a powerful antioxidant; but is resveratrol effective in humans?

  1. Quack watch says: don’t buy into the hype that resveratrol is effective in humans.
  2. WebMD claims that there would not be enough medical evidence to say that the average person should supplement with resveratrol to receive benefits.

Despite these recommendations the following evidence supports that resveratrol is indeed effective in humans.

Resveratrol effective in humans: high blood pressure patients

A 2017 study of high blood pressure patients examined resveratrol supplementation with two groups, 46 stage 1 hypertension patients and 51 stage 2 hypertension patients. Stage I hypertension had a systolic blood pressure of 140–159 mmHg and a diastolic blood pressure of 90–99 mmHg. Stage 2 hypertension was defined as a systolic blood pressure of 160–179 mmHg and a diastolic blood pressure of 100–109 mmHg. Each subgroup was divided into two groups, one receiving regular antihypertensive medication, and the other group receiving regular antihypertensive medication plus Evelor. Evelor is a micronized formulation of resveratrol. The trial lasted two years. The purpose of the trial was to determine the effect of resveratrol, which was added to the regular antihypertensive medication (or not) to see whether it had blood pressure lowering effects. The interesting result showed that the resveratrol addition was sufficient to bring the blood pressure down to normal levels with only one antihypertensive drug. The control group without resveratrol needed two or three drugs to get the blood pressure under control. In addition, liver function tests showed that resveratrol normalized negative side effects of the antihypertensive drug on the liver. Both liver enzymes, glutamate-pyruvate transaminase (SGPT) and gamma-glutamyl transferase (Gamma-GT) were normal in the group where resveratrol had been added.

Resveratrol effective in humans: diabetes patients

Resveratrol helps diabetes patients. Resveratrol, the bioflavonoid from red  wine is a powerful anti-inflammatory. This antioxidant has several other effects, which make it challenging to measure each effect by itself. This group of investigators managed to simultaneously measure these effects. They found that resveratrol lowered the C-reactive protein by 26% and tumor necrosis factor-alpha by 19.8%. Resveratrol also decreased fasting blood sugar and insulin; in addition it reduced hemoglobin A1C and insulin resistance. The recommended daily dose of resveratrol was 1000 to 5000 mg.

Resveratrol effective in humans: improves bone density

Resveratrol improves bone density in men: 66 middle-aged obese men with an average age of 49.3 years and a mean body mass index of 33.7 were recruited for this randomized, double blind, placebo-controlled trial. The purpose was to study whether there would be changes in bone turnover markers (LDH, an enzyme involved in bone turnover), but also whether bone mineral density (BMD) would increase. Resveratrol was given to a high group (1000 mg per day), a low group (150 mg) and a placebo (fake pills) were given to the third group. The end point was an elevation of the bone alkaline phosphatase (BAP). This was measured in the beginning of the study and at 4, 8 and 16 weeks. The high group of resveratrol had a 16% increase of the BAP throughout the study and a 2.6% in lumbar spine bone density (measured by a trabecular volumetric method). The low resveratrol group showed no bone restoring effect. MJ Ornstrup, MD, the lead investigator said that this was the first time that a clinical team has proven that resveratrol can potentially be used as an anti-osteoporosis drug in humans. She added that resveratrol appears to stimulate bone-forming cells within the body.

Resveratrol effective in humans: anti-aging effects

The Nurses’ Health Study showed that both a Mediterranean diet and resveratrol can elongate telomeres.

The fact that you can have a longer life with a Mediterranean diet is known for some time. But now a study has shown that the reason for a longer life is the fact that telomeres get elongated from the Mediterranean diet. Telomeres are the caps at the end of chromosomes, and they get shorter with each cell division. This is the normal aging process.

The finding of elongated telomeres comes from the ongoing Nurses’ Health Study that started enrolling subjects in 1976. At that time 121 700 nurses from 11states enrolled in the study. In 1980 diet sheets were used to determine who was adhering to a Mediterranean diet. 4676 middle-aged participants were identified to qualify for this study. This diet consists of a combination of vegetables, legumes, fruits, nuts, grains and olive oil. Fish and lean meats were also consumed. The control group followed a regular diet. Between 1989 and 1990 blood tests were obtained to measure telomere length in white blood cells. It is known that smoking, stress and inflammation shortens telomeres. The lead author Marta Crous-Bou stated that overall healthy eating was associated with longer telomeres compared to the control group. But the strongest association was found in women who adhered to the Mediterranean diet when compared to the controls. For the best diet adherence score there was a 4.5 year longer life expectancy due to slowed telomere shortening.

Longer telomeres have been found to be associated with the lowest risk to develop chronic diseases and the highest probability of an increased life span. I have reviewed the importance of lifestyle factors in this blog where I pointed out that Dr. Chang found a whole host of factors that can elongate telomeres by stimulating telomerase. It has been shown in humans that increased physical activity elongated telomeres. So did vitamin C, E and vitamin D3 supplementation, resveratrol, a Mediterranean diet and marine omega-3 fatty acid supplementation. In addition higher fiber intake, bioidentical estrogen and progesterone replacement in aging women and testosterone in aging men, as well as relaxation techniques like yoga and meditation are also elongating telomeres.

Aging is due to shortening of telomeres. Elongation of telomeres by resveratrol leads to prolonged life (or anti-aging).

Resveratrol effective in humans: resveratrol and cancer

As this overview shows, it seems that several mechanisms of action give resveratrol the power to be an anticancer agent. Resveratrol is anti-proliferative and has anti-angiogenesis mechanisms. In addition resveratrol stimulates apoptosis, which is programmed cell death. All these actions together help resveratrol to have anticancer properties. Resveratrol can also be used in combination with other cancer treatments, which improves survival figures. As the link above explains, more cancer clinical trials with a variety of cancers and larger patient numbers are required, but many smaller clinical trials have already been very successful showing efficacy of resveratrol as a chemotherapeutic agent.

In this 2015 publication about malignancies and resveratrol an overview is given about the use of resveratrol and cancer treatment. It summarizes that the development of cancer is a multifactorial process that involves the 3 stages of initiation, promotion and progression. One of the cancer promoting factors is chronic inflammation. Resveratrol has been shown to be anti-inflammatory. At this point it is not clear how the animal experiments will translate into the human situation. More clinical observations are necessary.

Resveratrol effective in humans: cardiovascular disease

Resveratrol has beneficial effects on preventing hardening of the arteries, diabetes, various cancers and inflammatory conditions like Crohn’s disease and arthritis. As this link explains resveratrol also stimulates the antiaging gene SIRT1 by 13-fold. This confirms the anti-aging effect of resveratrol. This 2012 study has also confirmed that resveratrol from red wine is what is responsible for the “French paradox” (longer life expectancy despite high saturated fat intake).

Resveratrol effective in humans: polycystic ovarian syndrome 

Polycystic ovarian syndrome could be significantly healed with resveratrol in a randomized, double blind, placebo-controlled trial. It involved 30 subjects who completed the trial. 1500 mg of resveratrol or placebo were administered daily for 3 months. Serum total testosterone was decreased by 23.1% at the end of 3 months in the experimental group versus the placebo group. There was also a decrease of dehydroepiandrosterone sulfate of 22.2%. Fasting insulin level was reduced by 31.8%. At the same time insulin sensitivity was increased by 66.3%. The authors concluded that resveratrol had significantly reduced ovarian and adrenal gland male hormones (androgens). This may be in part from the drop in insulin levels and the increase of insulin sensitivity.

Resveratrol effective in humans: anti-arteriosclerotic effects in diabetics

A double blind, randomized, placebo-controlled study was done on 50 diabetics. The cardio-ankle vascular index (CAVI) was used to determine arterial stiffness. The purpose of this study was to determine the effect of resveratrol on the stiffness of arteries in a group of diabetics and compare this to a placebo. Diabetics are known to have premature hardening of the arteries (arteriosclerotic changes). After 12 weeks of taking 100 mg of resveratrol per day there was a significant reduction in arterial stiffness in the experimental group, but not in the placebo group. Blood pressure also decreased by 5 mm mercury (systolic) in the experimental group.

Resveratrol effective in humans: ulcerative colitis patients

56 patients with mild to moderate ulcerative colitis received 500 mg of resveratrol or placebo and were observed for 6 weeks. This was a randomized, double blind, placebo-controlled pilot study. Bowel disease questionnaires were used to assess the bowel disease activity before and after the treatment. The resveratrol group decreased the disease activity significantly, but it also increased their quality of life. Blood tests showed that this improvement occurred as a result of reducing oxidative stress by resveratrol.

Resveratrol effective in humans: Alzheimer’s disease prevention

Here is a study where 52 Alzheimer’s patients were divided into two groups; one group was given 200 mg of resveratrol for a number of weeks, the other group placebo pills. There was a significant improvement in memory tests in the resveratrol group and functional MRI scans showed better functional connectivity in the hippocampi of the subjects. It is known that the hippocampus is the seat for short-term memory, which is lost in Alzheimer’s patients.

Resveratrol Effective In Humans

Resveratrol Effective In Humans

Conclusion

Resveratrol has a long history of showing evidence of improving health. It does so by countering oxidation of LDL cholesterol, which lessens hardening of arteries. This prevents heart attacks and strokes. Resveratrol is also a powerful anti-inflammatory, which helps patients with diabetes, with Crohn’s disease and arthritis. There is even a cancer preventing effect of resveratrol because of anti-proliferative and anti-angiogenesis effects as well as stimulating apoptosis. Because of these combined anticancer properties resveratrol is a chemotherapeutic agent that can be combined with conventional anticancer drugs.

There are enough randomized, double blind, placebo-controlled trials in humans to show that resveratrol is effective in preventing and treating several disease conditions. The medical establishment claims that there would not be enough medical evidence to say that the average person should supplement with resveratrol to receive health benefits. After my review outlined above I come to the opposite conclusion. It is quite clear that resveratrol has several important healing properties. It can improve diabetes; prevent hardening of arteries, lower blood pressure, attack osteoporosis and prevent Alzheimer’s disease. I have been taking 500 mg of resveratrol daily for years. It has not harmed me.

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Jul
01
2017

Advanced Glycation End Products (AGEs)

Advanced glycation end products (AGEs) form when food is cooked at high temperatures. Sugar molecules react with proteins crosslinking them and changing how they function. It prevents proteins from doing their job. Glycation also causes inflammation, which damages mitochondria, the power packages inside cells that provide the body with energy. Overall AGEs lead to premature aging, which comes from the toxic protein reactions. Advanced glycation end products accumulate as glycated proteins in the tissues of the body. This leads to mitochondrial dysfunction.

Effect of advanced glycation end products (AGEs) on the body

The following tissues are frequently affected by the toxic effect of AGEs.

  • The accumulation of AGEs can cause kidney disease and kidney failure (renal failure). In this case the kidneys no longer filter the blood to excrete waste. Hemodialysis may be required.
  • Joint cartilage is damaged by AGEs so it can no longer handle stress and joint stiffness sets in. AGEs are now recognized as a major cause of osteoarthritis.
  • Cross-linked proteins from AGEs can cause Alzheimer’s and Parkinson’s disease. Damaged proteins accumulate in brain cells that disable and kill them eventually.
  • Glycation of LDL particles has been well documented as an important cause of increasing the plaque formation in arteries by LDL. Glycated LDL is much more susceptible to oxidation than regular LDL. Oxidized LDL causes damage to the lining of the arteries and destroys endothelial nitric oxide synthase. This is a critical enzyme, which is involved in maintaining vasodilatation and blood flow. Once LDL has become glycated, it is deformed and LDL receptors can no longer recognize it. This means that glycated LDL continues to circulate in the bloodstream where it contributes to the atherosclerotic process. It forms a plaque which becomes a reason for heart attacks and strokes. Glycation of LDL is particularly common in patients with diabetes.
  • Glycation of the skin sensitizes the skin to UV light damage. It triggers oxidative stress that increases the risk of skin cancer.
  • Glycation damages our eyes. It causes clouding of the lens (cataracts) and it damages the retina. Macular degeneration can ultimately cause blindness.
  • When glycation affects the discs in the spinal cord, this can cause disc protrusions and disc herniations. Often the spinal nerves that are nearby get injured causing limping and leg or arm weakness.

Nutrients to counter AGEs

There are nutrients that can slow down the rate of glycation and as a result will halt the aging process.

Benfotiamine

Benfotiamine is a fat-soluble form of the water-soluble vitamin B1 (thiamine). It has been shown to reverse glycation in cell cultures and in humans.

As a result the damage to the cells that are lining arteries is reduced. Benfotiamine also counters diabetic neuropathy, retinopathy and nephropathy.

Pyridoxal 5’-phosphate

Pyridoxal 5’-phosphate is a metabolite of vitamin B6. It is similar to benfotiamine in that it counters glycation and dissolves deposited AGEs. It is particularly useful to stop fat and protein glycation. In diabetic patients lipid glycation is often a problem as these authors have shown. Pyridoxal 5’-phosphate traps glucose breakdown products before they become part of glycation reactions.

Carnosine

Carnosine is a dipeptide, made up of the amino acids histidine and beta-alanine. It is found in higher concentration in muscle and brain tissue. It scavenges for free radicals and prevents AGE formation. It is preventing both lipid glycation and protein glycation. This publication states that carnosine can play a role in preventing Alzheimer’s disease. As protein crosslinking is prevented with carnosine, tangled protein clumps cannot accumulate and cause Alzheimer’s disease.

Carnosine also reduces blood lipid levels and stabilizes atherosclerotic plaques. This reduces the risk of plaque rupture, which can cause a heart attack or stroke.

Carnosine also has a mitochondria stabilizing function resisting the destructive effects of oxidative stresses.

Luteolin

Luteolin is a bioflavonoid, which can be found in many plants. It has anti-inflammatory effects and works by suppressing the master inflammatory complex, called NF-kB.  NF-kB triggers the production of multiple cytokines and is associated with many cancers, chronic diseases, autoimmune diseases and septic shock. Kotanidou et al. did an experiment where they injected mice with Salmonella enteritis toxin, either with or without luteolin protection. Without luteolin only 4.1% of the mice survived on day 7. With luteolin protection 48% were alive on day 7.

Luteolin has been shown to be effective as an anti-inflammatory in the brain, the blood vessel lining, intestines, skin, lungs, bone and gums.

All these four supplements are available in the health food store. They work together and would be recommendable in diabetic patients where glycation is most prominent. But these supplements are also useful for older people who want to slow down the aging process in general.

Nutrients to slow down mitochondrial aging

Glycation is linked to mitochondrial deterioration and dysfunction. It accelerates aging in every aspect. AGEs (advanced glycation end products) crosslink proteins, lipids, but also damage enzymes and DNA. Mitochondrial energy production is slowed down by glycation. The end result is a lack of energy and slower repair processes, which all depend on mitochondrial energy production. The following supplements have shown some merit in reversing this process.

Pyrroloquinoline quinone (PQQ)

PPQ is a supplement that is known to produce new mitochondria in cells. This helps the energy metabolism of aging cells to recover.

Taurine

Taurine is an amino acid that is found abundantly in heart and skeletal muscles cells, brain cells and cells of the retina. These are areas in the body with high metabolic rates that can burn out mitochondria. Taurine regulates enzymes in mitochondria that harvest energy from food substances. In patients who experience accelerated aging, a lack of taurine can produce an energy crisis. But supplementation with taurine can rescue the cells by reducing oxidative stress and restoring the function of mitochondria in cells that are aging. Brain cells were putting out new shoots, called neurites when taurine was given as a supplement. This helps to improve brain connection, and preserves memory and cognition.

R-lipoic acid

R-lipoic acid helps with mitochondrial function by being involved with extracting energy from foods. When R-lipoic acid is given to aging animals, their metabolic function improves, the mitochondria become healthier and there are less oxidative stress-inducing byproducts. It protects their liver, heart and brain cells from oxidative stress in their mitochondria. It is becoming known as an energy-giving supplement.

Advanced Glycation End Products (AGEs)

Advanced Glycation End Products (AGEs)

Conclusion

Sugar overconsumption and overcooking food can cause advanced glycation end products (AGEs) where lipids and proteins get cross-linked. This leads to premature loss of organ function. The mitochondria are also slowed down. This creates prematurely aging. Fortunately there are a few supplements like benfotiamine, pyridoxal 5’-phosphate, carnosine and luteolin. They protect against glycation. Mitochondria can also be protected by PPQ, taurine and R-lipoic acid. Although we cannot stop the aging process, avoiding sugar and stopping to consume overcooked food, such as barbecued meats and deep fried food is a sensible step in prevention.

With this approach and some supplements a lot can be done to slow down aging.

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Jun
10
2017

Dementia And Strokes From Diet Drinks

You can get dementia and strokes from diet drinks. This is what a recent study published on April 20, 2017 in the American Heart Association Journals has shown. Because of the bad press around sugary drinks more and more people have switched to diet drinks. But the authors of this study have found a correlation of consuming diet soft drinks (with artificial sweeteners), dementia and ischemic strokes.

How was the study done?

A community-based Framingham Heart Study Offspring cohort was followed for 10 years. There were two age groups they followed: mean age of 62 and mean age of 69. There were 2888 participants in the younger age group and 1484 participants in the older age group. The younger age group was followed to monitor for strokes, the older for dementia. During the observation time there were 97 cases of stroke (82 of them ischemic) and 81 cases of dementia (63 due to Alzheimer’s disease). Compared to the control group with no consumption of diet drinks, there was an increase of 296% of ischemic stroke and 289% increase of Alzheimer’s disease. This was the data based on consuming diet soft drinks for 10 years. Another control group had consumed sugar-sweetened beverages. They did not develop strokes or dementia (observation time too short). As can be seen under this link the popular press also reviewed the study.

What do we know about artificial sweeteners?

Here is a brief review of the most common sweeteners.

1. Saccharin

This sweetener’s history goes back to 1879 when the Russian chemist Constantin Fahlberg first noted experimenting with coal tar compounds that one of the end products, benzoic sulfanide, tasted sweet. In fact it was between 200 and 700 times sweeter than granulated sugar! But there were political struggles that accompanied this saccharin throughout the years. There were rumours that in rats saccharin could cause bladder cancer. The health authorities became concerned. This led to Congress passing the Pure Food and Drug Act in June of 1906, to protect the public from “adulterated or misbranded or poisonous or deleterious foods, drugs or medicines.” This was the precursor of the FDA that would examine all of the medical evidence and consider the pros and cons of sweeteners as well. President Roosevelt took saccharin for weight control to replace sugar. In 1908 Roosevelt felt he had to stop the actions of overzealous Dr. Harvey Wiley, chief of the U.S. Department of Agriculture’s chemical division,who was of the opinion that saccharin should be taken off the market. Dr. Wiley did not give up his fight and finally the FDA decided to ban saccharin in processed foods, but to continue to allow private sales of saccharin.

2. Cyclamate 

Cyclamate was detected in 1937. It was marketed first to achieve a better control of diabetes. Because of the reduction in sugar consumption it allowed diabetic patients to cut the amount of insulin required to control diabetes. Cyclamate did not have a bitter aftertaste, so it was mixed with saccharine at a ratio of 10 parts of cyclamate to 1 part of saccharin , which resulted in the creation of “Sweet ‘N Low. In 1958 the FDA gave cyclamate the GRAS designation: “generally recognized as safe”. The good fortunes of cyclamate did not last long: in 1969 damaging animal experiments showed that cyclamate/saccharin had caused chromosomal breaks in sperm of rats. Another study from 1970 showed bladder tumors in rats. Other studies showed lung, stomach and reproductive tumors in animal experiments with cyclamates/saccharin. The FDA wanted to shut down the sale of the Sweet N’ Low sweetener, but public pressure and the food processing industry forced the issue to be brought up in front of Congress. The compromise was to use a warning label: “Use of this product may be hazardous to your health. This product contains saccharin which has been determined to cause cancer in laboratory animals.” In the year 2000 and beyond a series of animal experiments and data from Denmark, Britain, Canada and the United States on humans showed there were no signs of bladder cancer from exposure to Sweet N’ Low. In 2000 Congress removed the warning labels.

3. Aspartame 

Aspartame was detected in 1965. James M. Schlatter, a chemist, was looking for anti-ulcer drugs, but noticed the intensely sweet flavor when he licked his fingers. This led to the newest sweetener by 1973. We know it by the trade names Equal, NutraSweet or Sugar Twin. As this sweetener consisting of the two amino acids phenylalanine and aspartic acid is metabolized in the body, it cannot be taken by people with phenylketonuria, with certain rare liver disorders or by pregnant women with high levels of phenylalanine in their blood, because it is not metabolized properly in those individuals. Any food made with aspartame has to carry that restriction on the label, a requirement by the FDA. In 1996 W. Olney and his associates presented research that implied that Aspartame would have caused brain tumors in rats. But later these experiments were disproven and studies from children with brain tumors showed “little biological or experimental evidence that aspartame is likely to act as a human brain carcinogen.”

4. Sucralose

Sucralose was detected in 1976 by insecticide researchers who looked for new types of insecticides. They found that chlorinated sugar worked as an insecticide. One of the researchers was astounded how sweet the chemical tasted. If you Google “Splenda and insecticide”, you have a hard time finding references regarding the history of sucralose, but 20 years ago I found a detailed description that explained how one of the chemists doing insecticide research accidentally tasted one of the research products, and it was about 600-times sweeter than table sugar. Here is one of the few references that explains that sucralose was discovered while looking for new insecticides. I have repeated the insecticide experiment myself in Hawaii where small ants are ubiquitous. Out of curiosity I took a package of Splenda from a coffee shop and sprinkled the contents in the path of ants. In the beginning the ants were reluctant to eat it, but after a short time they came and took it in. They slowed down, and finally they were all dead. A few hours later there were only shrivelled up dead ants left in the area where Splenda had been sprinkled. Proof enough for me that Splenda was developed as an insecticide and should not be consumed by humans! In the meantime Dr. Axe in the above references lists the side effects in humans: “Migraines, agitation, numbness, dizziness, diarrhea, swelling, muscle aches, stomach and intestinal cramps and bladder problems.” In the Splenda marketing scheme they decided to first introduce Splenda gradually into diabetic foods as a sweetener, then later sell it to the public at large. Don’t fall for it! It was a side product of insecticide research, and insecticides have the undesirable quality of being xenoestrogens, which block estrogen receptors in women. As a result estrogen can no longer access the body cells, including the heart. The final consequence for a woman is a higher risk for cardiovascular disease. This can cause heart attacks, strokes and cancer. In men estrogen-blocking xenoestrogens can cause breast growth and erectile dysfunction. Taken everything together Splenda seems to be too risky for its sweetness.

5. Other sweeteners

Other sweeteners researchers have not stopped looking for newer, better sweeteners. There is a number of sugar alcohols with less calories than sugar such as erythritol. Another common sugar alcohol is xylitol, used in chewing gum. The advantage is that these are natural sweet alcohols that exist in nature. Xylitol originated from birch wood and was touted to help tooth decay when you use chewing gum containing it. Karl Clauss and Harald Jensen in Frankfurt, Germany detected another sweetener, acesulfame potassium, also known by the names acesulfame K, Ace-K, or ACK in 1967 when they experimented with various chemicals. This is known under the brand name “Sweet One”, but is often disguised in processed foods together with other artificial sweeteners to mimic the taste of sugar.

6. Stevia 

Stevia has been used for over 400 years, particularly in South America. It grows like a small bushy herb with leaves that can be taken to sweeten foods.  With modern, reliable extracting procedures (Sephadex column) it is possible to separate the bitter component of stevia and discard it leaving stevia behind without any bitter aftertaste. In Japan stevia has been occupying 40% of the sweetener market. In Europe and North America there is a lot of competition with the above-mentioned sweeteners, mainly because of clever marketing techniques. In 2008 stevia received GRAS status by the FDA.

What does sugar in soft drinks do?

Sugar is an emotional topic that can get people caught up in heated discussions. The sugar industry and the sugar substitute industry have also powerful lobby groups that provide the Internet and the popular press with conflicting stories to convince you to buy their product. There is good data to show that sugary drinks cause heart attacks, strokes and diabetes. Let’s not forget the metabolism behind the various sugars and starchy foods leading to fat deposits, high triglycerides and high LDL cholesterol. Forget the emotions of severing yourself from your favorite fix and stick to a tiny amount of stevia that can replace the familiar sweet taste that you have become accustomed to from childhood onward. (At least this is what I do.) The only alternative would be to take the plunge and cut out any sweet substance altogether, which I am not prepared to do. If you can do it, by all means go ahead. For more details regarding the effects of sugar and starchy foods read the blog under this link.

Dementia And Strokes From Diet Drinks

Dementia And Strokes From Diet Drinks

Conclusion

The reason diet soft drinks have become so popular is that it had been proven in other studies in the past that sugary drinks could cause heart attacks and strokes. Now a new study revealed that diet soft drink consumption is associated with dementia and strokes. These drinks contained saccharin, cyclamate, aspartame or sucralose. They did not contain stevia, a natural sweetener because it is a natural, not a patented sweetener. It seems that companies’ profits are higher with chemical, patented sweeteners.

Looking back in time it seems perfectly legal that a company produces a chemical, patents it and sneaks it through the FDA channels for approval. The company then markets diet soft drinks that later are shown to produce dementia and ischemic strokes in much larger studies than were originally used to get FDA approval.

I have noticed that companies are now quietly introducing stevia, a natural sweetener to avoid potential legal problems down the road. Perhaps it is time to follow the Japanese lead where stevia is already occupying 40% of the sweetener market.

May
20
2017

Prevention Of Telomere Shortening

Dr. Mark Rosenberg gave a talk on prevention of telomere shortening. This was presented at the 24th Annual World Congress on Anti-Aging Medicine (Dec. 9-11, 2016) in Las Vegas that I attended. The detailed title was: “The Clinical Value of Telomere Testing”.

What are telomeres?

Telomeres are the caps at the end of chromosomes. They are very important in the aging process. Prematurely shortened telomeres are linked closely to all major diseases like cardiovascular disease, cancer, diabetes and more. Telomeres are also a measure of the aging process. Aging occurs due to a decrease of the number of cells in organs and/or because of a lack of functioning of these organs. Telomeres get shortened every time a cell divides. But when the telomeres are used up, there comes a time when cells can no longer divide. These cells become senescent cells or they enter apoptosis (programmed cell death).

The senescent cells can become a problem when they get transformed into cancer cells and their telomeres lengthen again. These cancer cells divide rapidly and this can become the reason why cancer patients to die.

What is the significance of telomeres?

Telomere dysfunction is the first sign that the telomeres are getting shorter in a person compared to the average telomere length in a comparable age group. This is not only important for aging, but also has clinical implications. The shorter telomeres are, the higher the risk for cardiovascular disease. Telomere length also provides prognostic information about the mortality risk (risk of dying) with type 2 diabetes and for many cancers. Many physicians incorporate a telomere blood test into periodic health checks, if the patient can afford it.

Interventions that help telomere length

Here are a number of things we can do to lengthen our telomeres.

  1. Rosenberg mentioned that the strongest effect on telomere lengthening comes from caloric restriction and weight loss. 80 years ago they showed at the Cornell University that rats put on calorie restriction had a 30% increase in their mean and maximum lifespan. Many research papers have confirmed that the same is true in man and that the common denominator is telomere lengthening.
  2. Next are regular physical activity, meditation, reduction of alcohol consumption and stopping to smoke.
  3. Taking antioxidants and omega-3 fatty acids regularly will also lengthen telomeres.
  4. Improving one’s dietary pattern by adopting a Mediterranean type diet that contains cold-pressed, virgin olive oil.
  5. Telomerase activators. Here is some background on the TA-65 telomerase activator, which is based on Chinese medicine. A one year trial was completed with 250 units and 1000 units of TA-65 per day. The lower dose (250 units) showed effective telomere lengthening, while the placebo dose did not. The 1000 unit dose did not show statistical significance.

Should you wish to take TA-65, only take 250 units per day, not more.

Cancer and telomeres

There is a strong correlation between cancer and telomere shortening. When cells are at the brink of dying toward the end of their life cycle the telomeres get shorter and shorter. This is the point where the cells can turn malignant. Certain genetic abnormalities help the malignant transformation, like 11q or 17q deletions or a p53-dependent apoptosis response. Once cancer cells have established themselves they activate telomerase in 85% of cases. In the remaining 15% of cancer cases telomeres are activated through telomerase-independent mechanisms. Here are a few examples.

CLL

CLL stands for chronic lymphocytic leukemia. It is a disease of the aging population. At age 90 people’s bone marrow cells have a telomere length of only 50% of the length at birth. This is the reason that in older age CLL is more common. Researchers observed a population segment and found that the shorter telomeres were, the poorer the overall prognosis and overall survival for CLL was.

Lung cancer

In patients with non-small cell lung cancer the telomerase activity was examined. When telomerase activity was present, the 5-year survival was only 55%. When telomerase activity was absent, the prognosis was 90% survival after 5 years.

Prostate cancer

  1. Telomere shortening in stromal cells was found to be associated with prostate cancer risk. Men with shorter telomere length in stromal cells had a 266% higher risk of death compared to men with normal telomere length.
  2. Another study took blood samples and determined the telomere length in lymphocytes (the immune cells). Those men who came down with prostate cancer within a year after the blood sample was taken had short telomeres. The risk for prostate cancer in these patients was 355% higher than in the prostate cancer negative controls.

Yet another study looked at surgical tissue samples from 596 men that

Underwent surgery for clinically localized prostate cancer. Patients whose samples showed variable telomere lengths in prostate cancer cells and shorter telomeres compared to prostate samples with less variable telomere length and longer telomeres had a much poorer prognosis. They had 8-times the risk to progress to lethal prostate cancer. And they had 14-times the risk of dying from their prostate cancer.

Breast cancer

Breast cancer is diverse and consists of cases that are genetically inherited (BRCA1 and BRCA2), but there are also cases where the cancer is local or more advanced (staging). In families with mutated BRCA1 and BRCA2 telomeres are significantly shorter than in spontaneous breast cancer. Increased telomerase activity in breast cancer cases is directly related to how invasive and aggressive the breast cancer is.

  1. One study was shown where blood leukocytes were analyzed for telomere length in 52 patients with breast cancer versus 47 control patients. Average telomere length was significantly shorter in patients with a more advanced stage of breast cancer than in early breast cancer. Mutated HER patients had the shortest telomeres. It follows from this that checking for the HER status and blood telomere testing adds to the knowledge of potential cancer development and prognosis.
  2. Short telomere length was associated with larger breast tumors, more lymph node metastases and more vascular invasion. More aggressive breast cancer cells have higher telomerase activity. More than 90% of triple negative breast cancers have short telomeres.

CNS disorders and telomeres

Dr. Rosenberg presented evidence that shorter telomeres are associated with dementia. But dementias with Lewy bodies and Alzheimer’s disease are also linked to short leukocyte telomeres. The length of blood telomeres predicts how well stroke patients will do and how people with depression will respond to antidepressants.

Cardiovascular disease and telomeres

Our blood pressure is kept constant through the renin-angiotensin-aldosterone system. When this system is not stable, our blood pressure shoots up and causes cardiovascular disease. This is tough for the heart, as it has to pump harder against a higher-pressure gradient. A study of 1203 individuals was examining the connection between leukocyte telomere length and renin, aldosterone and angiotensin II activity. It concluded that oxidative stress and inflammatory responses affect the telomere length of leukocytes and that the more stress there is in the renin-angiotensin-aldosterone system, the more cardiovascular disease develops. The conclusion of the study was that the overall cardiovascular stress leads to shortening of leukocyte telomeres.

Prevention Of Telomere Shortening

Prevention Of Telomere Shortening

Conclusion

Telomere length testing from a simple blood test will become a more important test in the future as hopefully the cost comes down (currently about 300$). It can predict the general aging status by comparing a single case to the general telomere length of the public. But it can also predict the cancer risk, risk for mental disease and cognitive deficits (Alzheimer’s disease). In addition your cardiovascular status is also globally assessed with this test. What can be done, if the test comes back with short telomeres?

It allows you to change your lifestyle and adopt a healthy diet. You can exercise regularly, take antioxidants and meditate. There are even telomerase activators that are gradually becoming more known. They lengthen the telomeres. The cost of telomerase activators will likely still be a problem for some time. All in all telomere length tests are here to stay, but effective intervention at this point is largely limited to healthy lifestyle choices. This is good news: healthy lifestyle choices like non-smoking, exercise and avoiding non-processed foods are either free or have a reasonable price tag. Telomerase activators are big business and at this point not really affordable!

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.

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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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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
02
2017

Gut Bacteria Can Protect Your Brain

The neurologist, Dr. David Perlmutter gave a keynote address where he pointed out that gut bacteria can protect your brain. The topic of his actual talk was “Rewrite your brain’s destiny” and the venue was the 24th Annual World Congress on Anti-Aging Medicine (Dec. 9-11, 2016) in Las Vegas. Many of the talks centered around the gut microbiome. In this talk Dr. Perlmutter stressed the fact that the right mix of gut bacteria will protect your brain, while the wrong mix can make you sick. There were many slides, but too much information to mention all of details of the talk here. I will summarize the broad outline of Dr. Perlmutter’s presentation and emphasize the practical implications this has for everyday life to prevent degenerative brain diseases.

A few facts

  1. Did you know that the brain uses 25% of the body’s energy, but has only a 3% of the body’s weight?
  2. The gut flora has trillions of gut bacteria with its own DNA material. 99% of the DNA material in our body comes from the gut bacteria and the bacteria on our skin surface; only 1% of the entire DNA in the body is your own DNA. We are eating for 100 trillion bacteria, but if they are good bacteria they provide us with important vitamins and they produce molecules that stimulate our immune system.
  3. This means we better have bacteria in our guts that are friendly, not the bad bacteria that can cause us problems. An Italian study determined the gut flora of children in central Africa (Burkina Faso) and compared the gut flora to children from developed countries in Europe. There was a significant difference with the African children having a healthy microbiome in the gut and the children from developed Europe having unhealthy gut bacteria. This is important new information. Many other research papers have established that leaky gut syndrome and autoimmune diseases are linked to dysbiosis, which is the name for the unhealthy microbiome in the gut.

Chronic inflammation

Dr. Perlmutter showed several slides where literature was cited showing that chronic inflammation in the civilized world is increasing. He also showed that dysbiosis (unhealthy gut bacteria taking over) is also increasing. On several slides Dr. Perlmutter showed that in civilized countries like Iceland, Denmark, Germany, the US, Japan and others the bacterial diversity of the gut bacteria in people was vastly reduced compared to the diversity of gut bacteria of people in Kenya, Ethiopia, Nigeria or rural India. The same countries that have diminished gut bacterial diversity (dysbiosis) also have the highest prevalence of Alzheimer’s disease. On the other hand the same countries with diverse gut bacteria have a low incidence of Alzheimer’s disease. When infestation with parasites was examined there was also a parallel between increased parasitic stress and low Alzheimer’s disease rates, again in countries like Kenya, Ethiopia, Nigeria or rural India. The same countries where gut dysbiosis was present the parasitic infestation was low.

Further research has established that gut dysbiosis leads to an inflammatory condition of the gut where lipopolysaccharides (LPS) from gut bacteria are absorbed causing inflammatory reactions within the body.

At the same time this leaky gut syndrome can cause obesity and leakage in the gut/brain barrier as indicated in this link. The result is neuroinflammation, cognitive impairment and vulnerability to develop Alzheimer’s disease. Our most dreaded brain diseases come from inflammation: Alzheimer’s, Parkinson’s disease, autism, multiple sclerosis etc. These are degenerative brain disorders due to chronic inflammation. If you eat a lot of red meat, sausages and processed foods your gut microbiome will undergo negative changes. If you eat healthy food with lots of vegetables, fruit and you cut out sugar and too many starches, you have a healthy microbiome, which develops a robust immune system. We have to rethink the gut/brain connection and learn how to prevent these chronic illnesses.

Obesity and gut dysbiosis

In the link above it was shown that obesity is associated with inflammation. It was also shown with MRI scans that the part in the brain, called hippocampus was shriveled up (atrophied). This is a typical sign of dementia and Alzheimer’s disease. The investigators also confirmed with mental health functional tests that these patients had cognitive decline.

Another study also noticed that in a group of obese patients the hippocampus part of the brain was shriveled up the more obese people were. Obesity is associated with dysbiosis of the gut flora.

Practical application: the DASH diet and the Mediterranean diet are both healthy, balanced diets, strikingly different from the Standard American diet. In a study the hypothesis was tested whether the DASH diet and the Mediterranean diet would postpone dementia in a group of elderly patients. The answer was: yes, the hypothesis is true.

What does gut dysbiosis do?

It was shown in mice that chronic inflammation of the gut through ingestion of an irritant (dextran sodium sulfate) led to reduced new nerve growth in the hippocampus compared to control animals. It only took 29 days to show a marked difference between experimental and control animals in terms of reduced growth in the nerve cells of the hippocampus, the center of cognitive control.

The negative mediators were inflammatory kinins released from the gut wall and affecting the brain.

Antibiotic treatments and antibiotic residues in milk, milk products, meat, but also in all GMO foods are the irritants of the gut wall in humans. The antibiotics change the gut flora and lead to dysbiosis, which then causes gut wall inflammation and the cascade of events described above. The new finding is that GMO food contains RoundUp (they are “Roundup ready” crops). The herbicide Roundup was originally patented as an antibiotic and still leads to significant dysbiosis. Dr. Perlmutter urged the audience to buy organic food as the only method to reduce our exposure to Roundup. Roundup contributes to causing celiac disease and gluten intolerance in addition to exposure to the modern wheat (Clearfield wheat). The FDA is starting to do testing on foods for Roundup (glyphosate).

If things are sounding bad for Roundup, it only gets worse: Roundup has now been linked to causing cancer. In medicine it usually takes some time before definite action is taken. The agriculture industry is so deeply entrenched in the use of Roundup; I suspect that denial will be the first line of defense. My first line of defense in turn is to stick to organic food.

To sum up: Roundup and the Standard American diet lead to dysbiosis in the gut, which causes leaky gut syndrome. This causes inflammation with the release of cytokines and LPS from the gut wall to the blood. These substances cross the blood/brain barrier and lead to inflammation in the brain. This affects the hippocampus with the classical sign of shrinkage. But Parkinson’s disease, multiple sclerosis, autism in children and Alzheimer’s disease in older people are all caused by chronic inflammation. There are three more brain-related diseases that are related to gut inflammation: stroke, depression and attention deficit hyperactivity disorder (ADHD). Dr. Perlmutter spent some time explaining that antibiotic overuse even leads to an increase of breast cancer as a Danish study has shown. Antibiotic use showed a linear increase of breast cancer as a result of increased antibiotic amounts used. The highest group had a twofold risk compared to a control group with no antibiotic use. Dr. Perlmutter interpreted this to indicate that chronic gut inflammation can even cause a disease like breast cancer.

What can we do to diversify our gut bacteria?

  1. Exercise: A recent study has shown that regular exercise is associated with a diversified gut flora. The reason seems to be the production of butyrate with exercise, which leads to a diversified gut flora. There are reduced LPS levels (lipopolysaccharides from gut bacteria) in people with a higher fitness score.
  2. Eat a DASH diet or the Mediterranean diet as indicated above.
  3. Avoid GMO foods because of the presence of Roundup, which functions like an antibiotic and leads to gut bacteria dysbiosis.
  4. Remember “Antibiotics are weapons of mass microbial destruction”. If you need to take them be careful that you rebuild your gut flora with probiotics. Use of antibiotics increases the risk of type-2 diabetes by 1.53-fold. It also causes a quadrupling of Alzheimer’s disease.
  5. A woman should consider natural childbirth whenever possible, as with a vaginal birth the child is “anointed with gut bacteria”. Vaginally delivered children remain healthier than children delivered by Cesarean section for several years.
  6. Acid-suppressing medications and NSAIDs (anti-inflammatory medication for arthritis) can also lead to dysbiosis. Proton pump inhibitors increase the risk of Alzheimer’s disease by 44%.
  7. Prebiotic fiber can prevent Alzheimer’s. Probiotics do the same.
  8. Avoid sugar: even the Oompa Loompa knew that “If you eat sugar, you get fat” as this YouTube video shows. And obesity is associated with gut dysbiosis with the associated higher risk of degenerative brain diseases.
  9. Take magnesium supplements (250 mg twice per day) and DHA from fish oil capsules. It stabilizes your brain metabolism.
  10. In severe, persistent cases of gut dysbiosis a fecal transplant can be considered by your gastroenterologist. This procedure is done in more than 500 hospitals in the US.
Gut Bacteria Can Protect Your Brain

Gut Bacteria Can Protect Your Brain

Conclusion

The diversity of gut bacteria is immensely important. As discussed, in rural areas of the world there is gut bacteria diversity. In civilized parts of the world dysbiosis of the gut flora frequently occurs. This can lead to gut inflammation and the inflammation eventually gets internalized and can even reach the brain. These are the points to remember: exercise; avoid GMO foods, use prebiotics and probiotics. Avoid antibiotics; also avoid meat from animals that were fed antibiotics for faster growth. Don’t eat processed foods and avoid sugar. A healthy gut creates a healthy body, and this includes a healthy brain as well.

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