Feb
02
2019

Hormones Helping In Menopause

Dr. Filomena Trindade presented a talk about hormones helping in menopause. This talk was part the 26th Anti-Aging Conference of the American Academy of Anti-Aging Medicine in Las Vegas from December 13 to 15, 2018. The exact title of her talk was “Women and cognition: insulin, menopause and Alzheimer’s”. Above the age of 80 Alzheimer’s disease in women becomes much more common compared to men. PET scans of the brain of postmenopausal women in comparison to PET scans of premenopausal women, often show more than 30% slow down of metabolism after menopause. Literature regarding that finding showed that it was mostly the decline in ovarian estrogen production that was responsible for the slow down in brain metabolism. Other factors that lead to Alzheimer’s disease are central adiposity (abdominal) and inflammation in the body.

Brain insulin resistance and Alzheimer’s

Older women with Alzheimer’s have more IGF-1 resistance and IGF-1 dysfunction. Other studies showed that minimal cognitive impairment (MCI) progressing into Alzheimer’s disease (AD) might be due to type-2 diabetes. One of the studies stated the following:

“We conclude that the term type 3 diabetes accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both type 1 DM and type 2 DM.“

Another publication said that type 3 DM is a neuroendocrine disorder that represents the progression of type 2 DM to Alzheimer’s disease.

Dr. Trindade presented several hormone studies in postmenopausal women who started to develop Alzheimer’s disease. Older women with existing Alzheimer’s did not respond to estrogen hormone replacement. They did not recover with regard to their memory loss. However, younger women who just entered menopause responded well to estrogen hormone replacement and many recovered from their memory loss.

Hormone changes in menopause

There are a number of hormones that experience changes with the onset of menopause. Estrogen production ceases in the ovaries. The production of progesterone in the ovaries also ends. In addition thyroid and adrenal gland hormone production decreases. Often insulin production is increased, but insulin resistance is present at the same time.

Stress can interfere with progesterone and aldosterone production as pregnenolone is the same precursor molecule for both hormones.

How stress interferes with Selye’s general adaptation syndrome

Stage 1 of Selye’s adaptation syndrome, called arousal, involves elevation of cortisol and DHEA. When stress is over, the patient recovers on his/her own.

Stage 2 is the adaptation stage, where cortisol is chronically elevated, but DHEA is declining. The patient feels stressed, has anxiety attacks and may experience mood swings and depressions.

Stage 3 is the exhaustion stage. The underlying cause of this stage is adrenal insufficiency. Both cortisol and DHEA blood levels are low. Patients often suffer from depression and chronic fatigue.

Other hormones and menopause

DHEA and cortisol (stress) have the same precursor (pregnenolone). This means that when a patient is stressed, DHEA production tends to suffer as most of the pregnenolone is used for the production of cortisol.

Dr. Trindade spent some time explaining the complicated details of thyroid hormones during menopause. In essence stress can interfere with the normal metabolism of thyroid hormones with respect to T3, T4 and reverse T3. The end result is that not enough functioning thyroid hormones are present and hypothyroidism may develop.

Both estrogen and progesterone are lower in menopause. In a longitudinal French study with over 80,000 postmenopausal patients the women that received replacement with bioidentical progesterone and estrogen did the best in terms of low Alzheimer’s rates and lower heart attack rates. You achieve optimal Alzheimer’s prevention best starting hormone replacement at the time when menopause starts. You need both estrogen to control hot flashes and to give you strong bones, and progesterone for preservation of your brain, your hair growth and a good complexion.

Hormones Helping In Menopause

Hormones Helping In Menopause

Conclusion

Hormones are missing in menopause and this becomes the starting point for many postmenopausal complaints of patients. The sooner the physician does blood tests to diagnose hormone deficiencies, the better. Various studies showed that the best result in terms of Alzheimer’s prevention is possible, when estrogen and bioidentical progesterone are replaced right at the beginning of menopause. This approach prevents neuroinflammation. There are no extracellular beta amyloid protein deposits and no intracellular tau protein deposits that typically are present with Alzheimer’s disease. In addition the cardiovascular system stays healthier for longer. It contributes to preventing heart attacks and strokes. A longitudinal French study with over 80,000 women who have received treatment with a combination of estrogen and bioidentical progesterone have excellent survival data. The women also enjoy excellent mental health, no cardiovascular complications and less cancer than controls without hormone treatment.

 

Jan
19
2019

Alzheimer’s disease is treatable with hormones

Dr. Thierry Hertoghe, an endocrinologist from Belgium, stated that Alzheimer’s disease is treatable with hormones. This talk was part the 26th Anti-Aging Conference of the American Academy of Anti-Aging Medicine in Las Vegas (from December 13 to 15, 2018).

First of all, Dr. Hertoghe treated many Alzheimer’s patients himself and noted that they often have multiple hormone deficiencies. Secondly, common deficiencies affect thyroid hormones, human growth hormone, estradiol for women and testosterone for men. But even vasopressin and oxytocin are hormones that may be lacking. Third,  after doing thorough blood tests to assess hormone levels, Dr. Hertoghe replaced what hormones were missing. Finally, many Alzheimer’s patients got their energy, muscle strength and memory back.

In the following I am summarizing what Dr. Hertoghe told the audience about the various hormones. Alzheimer’s disease is treatable with hormones. Later I provide the hormone doses that Dr. Hertoghe uses for replacement.

Progressive memory loss

Generally, patients who develop Alzheimer’s disease start losing short-term memory first, but in time they will also lose long-term memory. Often this disease process starts in the 60’s as age-associated cognitive impairment. In the 70’s it may progress further to mild cognitive impairment, only to take off in the 80’s as Alzheimer’s disease. The astute clinician may order some screening blood tests in the 60’s and 70’s. In a male low testosterone, low DHEAS and low thyroid hormones may be present. Certainly, blood tests will show this readily. Frequently, in women low estradiol, low thyroid and low DHEAS may also be present. The reason this is important is that simple hormone replacement can return a person back to normal. Yes, this is right: hormone replacement can bring a person with age-associated cognitive impairment or mild cognitive impairment back to normal! In other words, Alzheimer’s disease is treatable with hormones.

Hormones important to monitor with Alzheimer’s disease

There are 6 hormones that are important for memory restoration in Alzheimer’s patients: IGF-1 (and growth hormone), thyroid hormones, estrogen and testosterone, vasopressin (and oxytocin) and pregnenolone. However, as Alzheimer’s patients often have sleep problems, another important hormone is melatonin.

Oxytocin to calm down aggressive Alzheimer’s patients

Notably, Dr. Hertoghe found that Alzheimer’s patients often are restless and can be aggressive. This makes it difficult to care for them in a home. Oxytocin is the hormone of trust, affection, sociability and concerns about others. It calms down aggressiveness. But with oxytocin treatment the Alzheimer’s patient feels better, becomes friendly, cooperative and warm-hearted.

As an illustration Dr. Hertoghe gave an example of one of his 80-year old patients with aggressive Alzheimer’s disease. She became unmanageable for her non-married son and other contacts. 5 IU of oxytocin sublingually changed this woman into a friendly, compassionate, warm-hearted woman, and the aggressiveness disappeared completely.

Insomnia in Alzheimer’s patients

About 45% of Alzheimer’s patients develop “sundowning”. When the sun goes down they start getting hyperactive, develop unacceptable behaviors and they become restless. Research papers showed that blood melatonin levels are low in these patients. Indeed, this is why they respond very well to small amounts of melatonin at bedtime. As a conclusion, within only a few days of starting this, their sundowning disappears, and they become easier to look after.

Dr. Hertoghe provided material from several research papers that showed that Alzheimer’s patients are often deficient for melatonin. Replacement with varying doses of melatonin solved even more complicated insomnia problems.

Melatonin is a powerful anti-oxidant. Interesting animal experiments have shown that melatonin has memory-enhancing properties. Researchers believe that melatonin improves the extracellular senile plaques with amyloid-beta peptide accumulation (first of 2 Alzheimer’s lesions). In addition melatonin also decreases the intracellular neurofibrillary degeneration tangles, the second of the two specific Alzheimer’s lesions.

IGF-1 and human growth hormone

Several studies have shown that Alzheimer’s patients have a significant drop in IGF-1 levels and growth hormone levels. This affects their short-term and long-term memory. Serum IGF-1 has an inverse correlation with cognitive impairment. Dr. Hertoghe said that IGF-1 treatment in Alzheimer’s patients increases their brain volume, increases the functional network of neurons in the brain and increases memory.

Brain atrophy in Alzheimer’s patients from chronically depleted IGF-1

Dr. Hertoghe showed a slide of a normal brain with a view from the outside and a cross section view of the brain. The same slide contained the view of an Alzheimer’s patient’s brain. It showed brain atrophy resulting in a much smaller brain and the cross section displayed an increase of the hollow spaces (e.g. the third and forth ventricle). He stressed that in his view the brain shrinkage of Alzheimer’s patients is due to prolonged low levels of IGF-1. This in turn is due to a lack of production of human growth hormone.

With IGF-1 treatment the serum IGF-1 was increasing and the cognitive function in older adults recovered. Dr. Hertoghe provided many literature citations to support this, which I will not repeat here.

Case report of a male patient with Alzheimer’s disease

Dr. Hertoghe presented one of his patients with Alzheimer’s. Lab tests showed that he had deficiencies of thyroid hormones, DHEA and testosterone. But despite replacement of these hormones he remained severely affected with Alzheimer’s. He did not remember his own name, could not go to the toilet on his own, spoke only a few words and suffered from severe fatigue. He received 4 injections around his eyes with IGF-1 and mesotherapy from his doctor (described below) with human growth hormone and IGF-1. Within a few weeks he had a complete reversal of his cognitive decline. He could return to his professional driving career doing halftime work with a delivery van in the city. He could read a newspaper and understood what he was reading. Alzheimer’s disease is treatable with hormones.

Thyroid hormones

According to Dr. Hertoghe thyroid hormones help to establish short-term and long-term memory and treat the apathetic depression in Alzheimer’s patients. Many Alzheimer’s patients are hypothyroid.With this deficiency they have swollen lower eyelids, a puffy face and paleness of the face. In a 1990 study a group of Alzheimer’s patients had 26% lower T3 levels when compared to normal controls. Many patients with hypothyroidism have memory loss, before their deficiency is corrected. Dr. Hertoghe stated that 13% of all dementia cases are reversible by proper thyroid hormone treatment.

Estradiol can improve long-term memory loss

Research showed that estradiol could improve long-term memory in dementia and Alzheimer’s disease cases. Many female Alzheimer’s patients are deficient in estrogens. If they do, they have dry eyes, a pale face and thin, dull hair. In a 2005 study 33 control women were compared to 48 women with Alzheimer’s disease. The estradiol levels in the Alzheimer’s disease group showed significant depletion compared to the normal control group. There was no significant difference found with regard to progesterone, testosterone and LH&HSH levels. Another study showed that in cerebrospinal fluid of women with Alzheimer’s disease the estradiol level was significantly reduced while the beta-amyloid levels were significantly increased.

Dr. Hertoghe reviewed several studies that showed that symptoms of Alzheimer’s disease disappeared with estradiol supplementation. Both memory and mood responded to the treatments.

Men with Alzheimer’s disease are often testosterone deficient

Testosterone is important for long-term memory. Men in andropause report erectile dysfunction, general weakness and memory loss. The physician needs to be aware that the patient may be starting to develop Alzheimer’s disease. Dr. Hertoghe showed a slide based on a publication, which stressed that testosterone enhances memory. It increases brain blood flow and thickens the myelin sheets. Testosterone increases dendrite and synapses and in addition decreases amyloid beta-peptide production. Neurotoxicity is also reduced. The end result is improvement of Alzheimer’s in males with testosterone replacement.

Pregnenolone improves short-term memory

Pregnenolone gets synthesized in the brain, spinal cord and peripheral nerves. Dr. Hertoghe said that pregnenolone is a neurostimulating “neurosteroid”. Pregnenolone concentrations in brain tissue are about 25- to 35-fold higher than in the blood stream. Some cases of Alzheimer’s disease can come from a lack of pregnenolone and pregnenolone sulfate. Patients who have Alzheimer’s because of a lack of pregnenolone have blood levels that are 2.5-fold lower than pregnenolone levels in normal controls. When these patients are treated with pregnenolone, their memory improves. The mechanism of the effect of pregnenolone is by increasing acetylcholine by more than 50% in the hippocampus. It also protects the hippocampus from glutamate and amyloid beta. Pregnenolone improves short-term memory over a period of 3 to 4 months of treatment.

Vasopressin improves short-term and long-term memory loss

Postmortem studies on Alzheimer’s patients showed that there is decreased vasopressin in the brain cortex. In patients with alcoholic dementia (Korsakoff psychosis after recovery) there was decreased vasopressin in the cerebrospinal fluid. Often patients with diabetes insipidus have decreased vasopressin and are in danger of developing dementia. If not treated, they develop short-term and long-term memory loss. When treated with vasopressin or Desmopressin their memory recovers within 4 hours of starting therapy. Younger patients (50 to 73) do better with memory recovery than older patients (74 to 91).

Treatment details of hormone replacement for Alzheimer’s disease

Before hormone treatments are given to a patient it is important to do a battery of blood tests. This will help the physician to identify the missing hormones in a particular patient. Each of the missing hormones are then administered separately.

Oxytocin

This hormone can be given sublingually or intranasally. Sublingually 5-10 IU are given daily. With the sublingual approach 1 or 2 sprays are given daily. Each spray contains 8 IU of oxytocin. Improvement is visible within 2 to 5 days. A full recovery takes 2 to 3 months.

Melatonin

Most patients in the higher age group do no longer produce their own melatonin. With the oral route 1-3 mg are given every night before going to bed. An alternative is to use sublingual tables 0.5mg to 1.0mg at bedtime. The first improvement can be seen 2-5 days after the start of replacing melatonin, the full impact takes about 2-3 months from the start of the treatment.

IGF-1 and human growth hormone

Replacement of IGF-1 can be done by injecting IGF-1 or human growth hormone (HGH). HGH stimulates the liver to produce IGF-1. IGF-1 is somewhat cheaper than HGH. When IGF-1 is used, 0.3mg to 1mg is injected at bedtime. Progress is slow; the first improvement is visible at 2-4 months, it takes up to 24 to 36 months for a full recovery.

For severe memory impairment with Alzheimer’s, the doctor does a double treatment approach with both IGF-1 and HGH: first subcutaneous IGF-1 injections around the eyes 4 times per day (0.01mg each). Secondly, at the doctor’s office the doctor administers mesotherapy injections with 1mg of HGH and 1mg of IGF-1 and vasodilators 3 times per week. Two weeks later the doctor administers another course of mesotherapy. He may repeat this twice in 14-day intervals. Now the interval increases to monthly therapy for 3 months and finally every 3 to 4 months. The patient can use IGF-1 nose drops instead of subcutaneous IGF-1 injections.

Thyroid hormones

Dr. Hertoghe prefers desiccated animal thyroid hormone replacement as the T3/T4 ratio is best matched to what the ratio is in humans. Depending on the severity of thyroid hormone deficiency the patient takes 30-150mg of thyroid hormone every morning. Dr. Hertoghe starts with a low dose and slowly increases the dosage. Clinical progress is very slow. It takes until the second month before the first improvement takes place. Full improvement can take 8-12 months.

Estradiol

Replacement of estradiol in postmenopausal women with Alzheimer’s disease received ether more than 0.1mg per day or 0.625mg of conjugated equine estrogen daily. In both cases there were improvements of their memory and improvement on the Hamilton depression scale.

Dr. Hertoghe’s preferred way to treat postmenopausal women with Alzheimer’s disease is as follows. The first 25 days of each month he gives them 1-2mg of oral estradiol valerate each day and 100mg of micronized progesterone. If they prefer an estrogen cream, he gives them 1-3mg per day transdermal estradiol and 100mg micronized progesterone capsules.

The first improvement is visible after 2-4 months; there is further improvement the next 8-12 months.

Testosterone

There are two methods of how to do hormone replacement with testosterone, either by injection or as transdermal cream. The injection treatment uses 250mg of testosterone enanthate or cypionate every 2 -3 weeks. The patinet can also self-administer testosterone enanthate (50mg twice per week) for a more even blood level of testosterone. The transdermal approach involves 100-250mg transdermal, nanoliposomal testosterone daily.

The memory will improve 2-4 months into replacement therapy. The full improvement takes 8-12 months.

Pregnenolone

The replacement therapy is 100mg per day in the morning for the first 4 months. Then there is a dosage reduction to 50mg daily. Studies have shown that 30mg of pregnenolone is not enough to treat memory loss. Short-term memory improved after 3 to 4 months in about 75% of patients.

Vasopressin

The best vasopressin preparation to use is bio-identical vasopressin. It comes as 1 nasal spray with 10IU of vasopressin. Upon awakening the patient or caregiver applies 1-2 sprays into the nose. The patient receives the second dose 10 minutes before lunch by nasal spray.

Apart from hormones, lifestyle changes are also recommendable.

Alzheimer’s disease is treatable with hormones

Alzheimer’s disease is treatable with hormones

Conclusion

Who would have thought that Alzheimer’s disease could have anything to do with hormones? Dr. Hertoghe, the endocrinologist from Belgium did many hormone tests on Alzheimer’s patients and concluded that various degrees of hormone deficiencies can indeed cause Alzheimer’s disease. But what is more is that you can replace the missing hormones and see complete cures in patients with Alzheimer’s disease. Alzheimer’s disease is treatable with hormones. This is something conventional medicine can only dream of. At this point this hormonal approach is not yet mainstream medicine; but it would not be a surprise to me, if in 10 or 20 years interested physicians do this type of therapy routinely in their practice. When hormones are missing, replace them. When the memory is fading, think about testing for missing hormones! It will make a difference in the quality of life for the patient as well as for his family.

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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.

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Sep
02
2017

Resveratrol Effective In Humans

Resveratrol is 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

First of all, 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 1 hypertension had a systolic blood pressure of 140–159 mmHg and a diastolic blood pressure of 90–99 mmHg. Stage 2 hypertension had a systolic blood pressure of 160–179 mmHg and a diastolic blood pressure of 100–109 mmHg. Analysts divided both stage 1 and 2 subgroups 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.

Blood pressure lowering effect of resveratrol

The purpose of the trial was to determine the effect of resveratrol.  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 gammaglutamyl transferase (Gamma-GT) were normal in the resveratrol group.

Resveratrol effective in humans: diabetes patients

Diabetes patients can get help with resveratrol. 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. Another 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

Furthermore, 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. The researchers gave resveratrol to a high group (1000 mg per day), a low group (150 mg) and the third group received a placebo (fake pills). The end point was an elevation of the bone alkaline phosphatase (BAP). The investigators measured this in the beginning of the study and at 4, 8 and 16 weeks.

Difference between high and low dose resveratrol

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 serve 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

Finally, 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 common knowledge 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.

Important information from the Nurses’ Health Study 

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 11 states enrolled in the study. In 1980 participants filled in diet sheets to determine who was adhering to a Mediterranean diet. The researchers accepted 4676 middle-aged participants in this study. This diet consists of a combination of vegetables, legumes, fruits, nuts, grains and olive oil. They also consumed fish and lean meats. 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.

Slowed telomere shortening

The lead author Marta Crous-Bou stated that overall healthy eating was responsible for longer telomeres in comparison to the control group. But the strongest association was in women eating a Mediterranean diet in comparison to the controls. For the best diet adherence score there was a 4.5 year longer life expectancy due to slowed telomere shortening.

Resveratrol lengthens telomeres

Longer telomeres associated with the lowest risk to develop chronic diseases and the highest probability of an increase of the 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. Research in humans supports the notion that an increase in physical activity elongates 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

In addition, 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 is also useful in combination with other cancer treatments, which improves survival figures. As the link above explains, there is a need for more cancer clinical trials with a variety of cancers and larger patient numbers. Many smaller clinical trials have already been very successful showing efficacy of resveratrol as a chemotherapeutic agent.

Resveratrol is anti-inflammatory

Also, 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 anti-inflammatory qualities. 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. Furthermore,  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 confirmed that it is resveratrol from red wine that is responsible for the “French paradox” (longer life expectancy despite high saturated fat intake).

Resveratrol effective in humans: polycystic ovarian syndrome 

Similarly, 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. Each of the subjects received 1500 mg of resveratrol or placebo daily for 3 months. Measurements showed a decrease of serum total testosterone 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%.There was a reduction of the fasting insulin level by 31.8%. At the same time there was an increase of the insulin sensitivity 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

Most noteworthy, a double blind, randomized, placebo-controlled study was done on 50 diabetics. Arterial stiffness was determined by the cardio-ankle vascular index (CAVI). 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 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

Finally, 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. The researchers used bowel disease questionnaires 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 received 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. The hippocampus is the seat for short-term memory, which is not functioning normally 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. These combined anticancer properties make resveratrol a chemotherapeutic agent. It is also effective in combination with conventional anticancer drugs.

Resveratrol helps prevent hardening of arteries and cancer

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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Feb
11
2017

Genetic Switches To Treat Obesity And Diabetes

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

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

In the light of these studies the results showed that 80% of a long life (longevity) is due to a healthy lifestyle and 20% comes from genetics. In addition, there are powerful epigenetic factors that can slow down aging and that can interfere with the inflammatory process that causes heart disease, obesity and diabetes. Also, there are specific inflammatory markers, which blood tests can determine. As a matter of fact, one of the first inflammatory markers detected was the C-reactive protein.

What diseases are caused from inflammation?

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

Age-related diseases also due to inflammation

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

Human genetics are complicated

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

Obesity and genetic factors

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

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

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

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

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

As can be seen, there are still gaps of knowledge how obesity develops, what percentage is due to genetic factors and how much is due to other factors including diets.

Diabetes and genetic factors

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

Useful supplements

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

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

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

What Dr. Nora concluded is that healthy nutrition plays a vital role in preventing FTO gene expression. He talked about silencing genes, which good nutrition and supplements can do.

Silencing diabetes genes

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

Nutritional genetic modifiers

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

Functional foods with regard to obesity and diabetes

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

  • The lignans of flaxseed lower LDL cholesterol and total cholesterol.
  • The catechins of green tea prevent obesity, but also obesity-induced type 2 diabetes.
  • Saponins of fenugreek lower lipid peroxidation and increase the antioxidant level.
  • Soy proteins contain phytoestrogen, genistein and daidzein; this lowers cholesterol levels in the blood, prevents lipid peroxidation and also has antioxidant activity.
  • Banaba leaves extract contains corosolic acid and ellagitannins. These substances are able to lower glucose levels in the blood. It also has an anti-obesity effect.
  • Grapes and related products contain anthocyanin, flavan-3-ols and flavonols. They have blood pressure lowering qualities, lower blood fat levels and prevent hardening of the arteries.
  • Dark chocolate contains flavanols that are the main type of flavonoid found in it. Flavanols decrease blood pressure and make platelets in the blood less sticky. This prevents heart attacks and strokes. In addition these flavanols also decrease LDL cholesterol, which prevents hardening of the arteries.

Here are more items that help your health

  • Red wine, berries, pears, and apples: proanthocyanidins are the active polyphenols that make all of these fruit valuable. Proanthocyanidins prevent LDL cholesterol from oxidizing through their antioxidant effects, which in turn slows down hardening of the arteries. It reduces the inflammation associated with narrowing of blood vessels and normalizes the lining of arteries.
  • Onions contain two active ingredients, allyl propyl disulfide (which makes you cry when you cut onions) and S-methyl-cysteine sulfoxide. These substances have anti-diabetic effects and lower blood fatty substances.
  • Turmeric contains curcumin, which possesses antidiabetic properties.
  • Fruit and vegetables contain fiber, which lowers blood sugars and hemoglobin A1C.
  • Stevia from the stevia plant reduces blood sugars following a meal in patients with type 2 diabetes.

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

Genetic Switches To Treat Obesity And Diabetes

Genetic Switches To Treat Obesity And Diabetes

Conclusion

This was a whirlwind review of how a healthy diet, supplements, fruit and vegetables, exercise and other healthy lifestyles can overcome genetic and epigenetic traits. After reading about this huge line-up of substances that can contribute to your health, you may feel slightly overwhelmed. Are you going to get all these wonderful items from the health food store and live on a bunch of supplements? Of course this is not the fact! Some herbals can be extremely helpful to combat inflammation, such as curcumin.

The essential facts of treatment of obesity and diabetes

But the most essential fact remains very simple: to cut down sugar and too many starchy foods, as they will trigger suppressed genes to cause diabetes, obesity, heart attacks and strokes. We need to inform ourselves and stay vigilant to the fact how toxic processed foods are, and we have to cut them out in order to stay healthy. We can become much more resilient to health challenges than we may have thought possible.

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Dec
31
2016

What Works Against Alzheimer’s?

.Eli Lilly’s promising drug solanezumab failed; so, what works against Alzheimer’s? This drug was supposed to dissolve the amyloid deposits that function like glue and make the patients lose their memory. This phase 3 trial was to test the drug on patients to assess efficacy, effectiveness and safety. But instead it showed that the new drug did not stop the loss of memory.

Brain bleeding as a side effect of potential Alzheimer’s drug

Now all those who were hoping for solanezumab to be effective, will jump on another drug, aducanumab. Biogen from Cambridge, Massachusetts, has developed this drug. Out of 165 subjects only 125 completed preliminary studies. 40 patients who discontinued it, had negative side effects. These included fluid building up in the brain, which was thought to be due to removal of the plaques. But others, had brain bleeding.

Although the drug manufacturer is still hoping that aducanumab will work out as an anti-Alzheimer’s drug, I have my doubts. A drug that can have potential brain bleeding as a side effect does in my opinion not qualify as an anti-Alzheimer’s drug.

Factors that help prevent Alzheimer’s

1. Diet can be as effective as a drug in treating Alzheimer’s

In September 2015 researchers from Rush University published results of putting Alzheimer’s patients on the MIND diet. The MIND diet was a prospective study where 923 people aged 58 to 98 years participated. Researchers followed these people for 4.5 years. Three groups of diets were tested: Mediterranean diet, DASH diet and MIND diet.

The MIND diet study result

The adherence to the diet was measured: those who followed the diet very closely, other participants who were less diligent, and finally those who were not compliant with the diet. With regard to the MIND diet the group with the highest adherence to the diet reduced the rate of Alzheimer’s by 53% compared to the lowest third. This is like a highly effective Alzheimer’s drug! The second group still was able to reduce the rate of Alzheimer’s by 35%, which would be like a regular strength drug. The control diets were the DASH diet and the Mediterranean diet. The group that was strictly adhering to the DASH diet reduced Alzheimer’s by 39%, the group that was very conscientious in adhering to the Mediterranean diet reduced Alzheimer’s by 54%. The middle thirds of both control diets did not show any difference versus the lower thirds.

Findings of Alzheimer prevention by diet

The conclusion was that a strict Mediterranean diet had a very good Alzheimer prevention effect, as did a strict MIND diet. However, when patients did not adhere too well to a diet, the MIND diet was superior still yielding 35% of Alzheimer’s prevention after 4.5 years. The other diets, when not adhered to that well, showed no difference from being on a regular North American diet. Here is more info about the MIND diet.

Conclusion

Avoid the Standard American Diet. Adopt a Mediterranean diet and stick to it in a strict fashion or adopt the MIND diet. The other benefit is that there are no side effects!

2. Stress and Alzheimer’s

2010 study from Gothenburg University, Sweden examined 1462 women aged 38-60 and followed them for 35 years.

Psychological stress ratings went back to 1968,1974 and 1980. 161 females developed dementia (105 of them Alzheimer’s disease, 40 vascular dementia and 16 other forms of dementia). The risk of dementia was higher in those women who had frequent/constant stress in the past. The condition became more severe the more stress they had to face in the past. Women with exposure to stress on one, two or three examinations had higher dementia rates later in life in comparison to women who had no exposure to any significant stress. Specifically, dementia rates were 10% higher after exposure to one stressful episode, 73% higher after two stressful episodes and 151% higher after exposure to three stressful episodes.

Conclusion

Prevention of Alzheimer’s is possible by avoiding stress and seeking counselling when stress occurred .

3. Be creative, prevent Alzheimer’s and dementia

In an April 8, 2015 publication from the Mayo Clinic in Rochester, MN and Scottsdale, AZ 256 participants aged 85 years and older (median age 87.3 years, 62% women and 38% men) were followed for 4.1 years. Psychological tests measured mild cognitive impairment (MCI). At the time of recruitment into the study all of the tests for MCI were normal. As the study progressed it became apparent that there were various risk factors that caused the onset of MCI, which is the immediate precursor of dementia/Alzheimer’s disease.

The finding was that the presence of the genetic marker APOE ε4 allele carried a risk of 1.89-fold to develop MCI and later Alzheimer’s disease.

Further findings of the study

When patient showed signs of depression at the time of enrolment into the study, the risk of MCI development was 1.78-fold. Midlife onset of high blood pressure led to a 2.43-fold increase and a history of vascular disease showed a relationship of 1.13-fold higher MCI development. The good news was that four activities correlated with a lower risk of developing MCI with aging. When the person engaged in artistic activities in midlife or later in life the risk for MCI development 73% lower, involvement in crafts reduced it by 45% and engagement in social activities by 55%. In a surprise finding the use of a computer late in life reduced MCI development by 53%. These are very significant observations. This would be equivalent to highly effective anti-Alzheimer’s drugs.

Conclusion

If you stimulate your mind in older age, even browsing on the computer, this will help you to prevent Alzheimer’s disease.

4. Lifestyle factors contributing to Alzheimer’s

a) Sugar consumption: Sugar consumption and too much starchy food like pasta (which gets metabolized within 30 minutes into sugar) causes oxidization of LDL cholesterol and plaque formation of all the blood vessels including the ones going to the brain. On the long-term this causes memory loss due to a lack of nutrients and oxygen flowing into the brain.

b) Lack of exercise: Lack of exercise is an independent risk factor for the development of Alzheimer’s disease. Exercise increases the blood supply of the brain, strengthens neural connections and leads to growth of neurons, the basic building blocks of the brain. Exercise increases mood-regulating neurotransmitters like serotonin and endorphins.

c) Sleep deprivation leads to memory loss, but so does the use of aspartame, the artificial sweetener of diet sodas. Make your own homemade lemonade. Squeeze the juice of half a lemon. Add mineral water to fill an 8 oz. glass. Add a tiny bit of stevia extract for sweetening. Stir and enjoy. Stevia has been in use for thousands of years.

5. Hormone changes

A lack of testosterone in men and estrogen in women interferes with cognition and memory. For this reason it is important after menopause and andropause (=the male menopause) to replace what is missing with the help of a knowledgeable health professional.

Progesterone is manufactured inside the brain, spinal cord and nerves from its precursor, pregnenolone, but in women it also comes from the ovaries until the point of menopause. The myelin sheaths of nerves requires progesterone and progesterone also has a neuroprotective function. In menopausal women bioidentical progesterone is a part of Alzheimer’s prevention.

Melatonin is a hormone, a powerful antioxidant and a neurotransmitter at the same time. It helps in the initiation of sleep, stimulates the immune system and protects from the toxic effects of cobalt. Lab tests in Alzheimer’s patients found elevated values. In an aging person it is wise to use melatonin at bedtime as a sleep aid and to preserve your brain.

6. Genetic risk of Alzheimer’s

At the 22nd Annual A4M Las Vegas Conference in mid December 2014 Dr. Pamela Smith gave a presentation entitled ”How To Maintain Memory At Any Age”. She pointed out that there are about 5 genes that have been detected that are associated with Alzheimer’s disease and in addition the apolipoprotein E4 (APOE4). About 30% of people carry this gene, yet only about 10% get Alzheimer’s disease, which shows how important lifestyle factors are (in medical circles physicians call this the “epigenetic factors”) to suppress the effect of the APOE4 gene. She also stated that our genes contribute only about 20% to the overall risk of developing Alzheimer’s disease. This leaves us with 80% of Alzheimer’s cases where we can use the brain nutrients and hormones discussed above and exercise to improve brain function.

7. Vitamin D3 protects your brain from Alzheimer’s disease

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

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

What does vitamin D3 have to do with this?

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

Specifically, the findings were as follows.

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

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

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

8. Avoid sugar overload

We already mentioned sugar consumption under point 4. But here I am mentioning it again because of the insulin reaction. An overload of refined carbs leads to an overstimulation of the pancreas pouring out insulin. Too much insulin (hyperinsulinemia) causes hormonal disbalance and leads to diabetes type 3, the more modern name for Alzheimer’s. All starch is broken down by amylase into sugar, which means that anybody who consumes starchy food gets a sugar rush as well. Too much sugar in the blood oxidizes LDL cholesterol, which leads to inflammation in the body. The consequence of chronic inflammation are the following conditions: hardening of the arteries, strokes, heart attacks, Alzheimer’s due to brain atrophy, arthritis, Parkinson’s disease and cancer.

What Works Against Alzheimer’s?

What Works Against Alzheimer’s?

Conclusion

In the beginning we learnt about a failed phase 3 trial regarding an anti-Alzheimer’s drug. Next we reviewed several factors that can all lead to Alzheimer’s and that have been researched for many years. It would be foolish to think that we could just swallow a pill and overlook the real causes of Alzheimer’s disease. I believe there will never be a successful pill that can solve the increasing Alzheimer’s problem. It is time that we face the causes of Alzheimer’s. This means cutting down sugar to normalize your insulin levels.

Lifestyle changes necessary to avoid Alzheimer’s

We need to supplement with vitamin D3 because we know that it helps. For women in menopause or men in andropause it is time to replace the missing hormones with bioidentical ones. We need to handle stress and avoid sleep deprivation. And, yes we need to exercise regularly. Following a sensible diet like the Mediterranean diet or the MIND diet makes sense. And let us keep our minds stimulated. Chances are, when we do all of this that we will not need any Alzheimer’s pill. This is not good news for the drug companies, but will be very good news for you. Last but not least, there are no side effects, only health benefits!

Additional resource on how to preserve your memory.

Nov
12
2016

Stress Drives Our Lives

Every year the American Psychological Association (APA) monitors the American public how stress drives our lives. This yearly report has been compiled since 2007. About 75% of the people questioned reported that they have experienced moderate to high stress over the past month.

Symptoms when stress drives our lives

What kind of symptoms can stress cause? It can cause sleep deprivation, anxiety, headaches and depression. But there can be more symptoms from any disease that stress may cause. The “Stress in America” report from February 2016 shows on page 5 that unhealthy life habits are used by low-income Americans to cope with stress. A bar graph shows that watching television or movies for more than 2 hours per day is common. Another way of coping is to surf the Internet more often, take more naps or sleep longer. Eating more, drinking alcoholic beverages and smoking more are other unhealthy ways to cope with stress.

As the stressed person gains extra weight and eventually becomes obese, there is a higher rate of diabetes that can develop with all of its complications.

Causes of stress in our lives

The “Stress in America” survey was based on 3,068 adults in the US who completed the survey during August 2015. 72% were stressed out about financial issues. 22% of these said that they were extremely stressed in the past month as a result of money concerns. Other common concerns were work, the economy, family responsibilities and concerns about personal health. Average stress levels among Americans decreased when compared to 2007. On a 10-point stress score respondents rated their stress at 4.9 in 2016 compared to 6.2 in 2007. But according to the American Psychological Association this is much higher than a stress rating of 3.7 considered to be a healthy level.

Stress affects people from all walks of life, workers, women, young adults, students and those with lower incomes.

“Stress is caused by the loss or threat of loss of the personal, social and material resources that are primary to us” Stevan Hobfoll, PhD, a clinical psychologist from Rush University Medical Center said. “So, threat to self, threat to self-esteem, threat to income, threat to employment and threat to our family or our health…” is what causes stress.

Stress drives our lives causing disease

When stress is too much for our system, we are starting to see pathology develop. “Stress is seldom the root cause of disease, but rather interacts with our genetics and our state of our bodies in ways that accelerate disease” professor Hobfoll says. The following are common diseases that can result from chronic stress.

Heart attacks and strokes

In a 2015 Lancet study 603,838 men and women who worked long hours were followed for a mean of about 8 years with respect to heart disease or strokes. All of the subjects were free of heart attacks and strokes when they entered into the study. There were a total of 13% more heart attacks in those who worked extra hours in comparison to those who worked 40 hours per week or less. With respect to strokes there were 33% more strokes in those who worked long hours. Researchers noted a dose-response curve for strokes in groups with various workloads. Compared to standard working hours there were 10% additional strokes for 41-48 working hours, 27% for 49-54 working hours and 33% for 55 or more working hours per week.

Stress drives our lives and causes substance abuse

In order to cope with stress many of us treat daily stress with alcohol. It makes you feel good subjectively, but it can raise your blood pressure causing heart attacks and strokes down the road. A low dose of alcohol may be healthy, but medium and high doses are detrimental to your health.

Next many people still smoke, although scientists have proven long time ago that it is bad for your health. It can cause heart attacks, various cancers and circulatory problems leading to leg amputations.

Overeating is another common problem. Comfort food relieves stress, but it puts on extra pounds. As you know it is easier to put weight on than get it off. Being overweight or being obese has its own problems: arthritis in the hips and knees makes walking more difficult. The metabolic syndrome sets in, which is a characteristic metabolic change causing diabetes, high blood pressure, heart attacks, strokes and certain cancers. The more weight you carry, the less likely you are to exercise. This deteriorates your health outlook.

Diabetes

Stress causes too much cortisol secretion from the adrenal glands. This raises blood sugar, and when chronic can cause diabetes. In addition unhealthy eating habits associated with stress can cause weight gain and high blood sugars leading to diabetes.

In a 2012 California study 148 adult Korean immigrants were examined. They all had elevated blood sugars confirming the diagnosis of type 2 diabetes. They had a  elevated waist/hip ratio.

A high percentage of the study subjects had risk factors for type 2 diabetes. This included being overweight or obese and having high blood glucose readings. 66% of them said that they were feeling stressed, 51% reported feeling anxious, 38% said they were feeling restless, 30% felt nervous and 3% said they were feeling hopeless.

An Australian long-term follow-up study computed risk factors for developing type 2 diabetes. Stress was a major contributor to diabetes.

A 30-day episode of any anxiety disorder had a 1.53-fold risk to cause diabetes. A depressive disorder had a 1.37-fold risk to cause diabetes and posttraumatic stress disorder had a risk of 1.42-fold to cause diabetes.

Infertility

Stress changes hormones in women causing ovulation problems and infertility. 1 in 8 couples in America have problems getting pregnant. Physicians identified stress as at least a contributing factor. But in men stress can also reduce sperm count and semen quality as this study describes.

Alzheimer’s disease

A 2010 study from Gothenburg University, Sweden examined 1462 woman aged 38-60 and followed them for 35 years.

Psychologists assessed the stress score in 1968,1974 and 1980. 161 females developed dementia (105 Alzheimer’s disease, 40 vascular dementia and 16 other dementias). The risk of dementia was higher in those women who had frequent/constant stress in the past. Women who had stress on one, two or three examinations suffered from higher dementia rates later in life. Researchers compared this to women did not have any significant stress. Specifically, dementia rates were 10% higher after one stressful episode, 73% higher after two stressful episodes and 151% higher after three stressful episodes.

Remedies for stress

Before you can attempt to remedy stress, you must first detect that you are under stress. You can recognize this when you have problems sleeping, you suffer from fatigue, when overeating or undereating is a problem, and if you feel depressed. Others may feel angry or are irritable. Some bad lifestyle habits may also make you aware that you are under stress. You may smoke or drink more in an attempt to manage stress. Some people abuse drugs.

Here are some suggestions how to remedy stress:

  1. Seek support from family, friends or religious organizations. If you engage in drugs or alcohol overuse or you feel suicidal, it is best to seek the advice from a psychiatrist or psychologist.
  2. Engage in regular exercise. This produces endorphins, the natural “feel-good” brain hormone. This reduces symptoms of depression and improves sleep quality.
  3. Do something that increases pleasure, such as having a meal with friends, starting a hobby or watching a good movie.
  4. Positive self-talk: avoid negative thoughts like “I can’t do this”. Instead say to yourself “I will do the best I can”. Psychologists have developed a technique where they teach patients how to turn negatives into positives. Psychologists call this therapy “cognitive therapy”. You may want to seek the advice of a psychologist to have a few cognitive therapy sessions.
  5. Daily relaxation: you may want to use self-hypnosis, tai-chi exercises or meditation to reduce your stress levels.
Stress Drives Our Lives

Stress Drives Our Lives

Conclusion

Stress is very common. Diverse diseases like heart attacks, strokes, diabetes and Alzheimer’s disease can all be caused by stress. It is important to minimize the impact of stress by seeking family support and support from friends. Engaging in regular exercise will release endorphins and make you feel better. Relaxation exercises and seeking counselling can all help you to manage stress. You cannot ignore or simply tolerate this force in your life. Stress is indeed there, but we can make a difference by managing it to avoid that stress manages us.

Oct
29
2016

High Insulin Levels Can Cause Alzheimer’s

Research published in April 2016 shows that high insulin levels can cause Alzheimer’s. Alzheimer’s disease is more common in diabetics. But until recently nobody knew why there would be this association. Finally new research from New York University (NYU) has shed light on this puzzle. It seems like the key is an enzyme that breaks down insulin, called insulin-degrading enzyme (IDE). Melissa Schilling (no relation to me), an innovation professor at NYU has discovered the metabolic pathway between diabetes and Alzheimer’s disease. This finding has enormous implications regarding the prevention of Alzheimer’s, as I will discuss below. Here is a link to the original paper.

Background information about Alzheimer’s

Alzheimer’s disease affects about 5.2 million Americans and 44 million people worldwide. Above all, there is a progressive loss of cognitive functioning over a long period of time due to senile plaques in the cerebral cortex and the subcortical areas of the brain. These senile plaques consist of amyloid-beta substance and neurofibrillary tangles. This protein material is like glue, which prevents the neurons from working properly and certainly causes memory loss and the confusion, which is so typical for Alzheimer’s patients. Normally amyloid-beta is in solution and prevents lipoproteins in the brain from oxidizing. But when the insulin-degrading enzyme is busy breaking down high levels of insulin, these processes overload this enzyme system. Amyloid-beta experiences supersaturation, as the body does not eliminate it at a normal speed. Consequently, this leads to the glue-like deposits of amyloid-beta in Alzheimer’s brains.

A 2004 estimate for the direct cost of Alzheimer’s disease to the US amounted to  $214 billion. By 2050 this could go up to $1.5 trillion, if there will be no cure Alzheimer’s.

High insulin levels can cause Alzheimer’s, but other mechanisms too

Professor Schilling found in her research that there are four main malfunctions that can lead to high amyloid-beta in the brain of Alzheimer’s patients.

  1. First, with diabetes type1, when the patient does not receive enough insulin, the insulin-degrading enzyme in the brain is not working hard enough. This results in inadequate removal of amyloid-beta from the brain and neurofibrillary tangles of amyloid-beta accumulate.
  2. Second, IDE requires zinc as a co-factor to work properly in breaking down amyloid-beta. Zinc deficiency is quite common, particularly in older people. In this case insulin levels are normal, but the removal of amyloid-beta from the brain is inadequate, as IDE function has become lower.
  3. Furthermore, in early type 2 diabetes there are high insulin levels and there is a competitive inhibition of the elimination of insulin and amylin-beta. This is probably the most common form of getting Alzheimer’s disease.
  4. Finally, excess production of an amyloidogenic protein can lead to an overabundance of amylin-beta, which overwhelms the insulin-degrading enzyme.

What treatment options are there for Alzheimer’s disease?

These four mechanisms from above have several implications as follows.

  1. If a type 1 diabetic patient is insulin deficient, intranasal insulin would be beneficial.
  2. If the patient has type 2 diabetes, intranasal insulin or insulin by injection would be the wrong approach. As stated earlier, there is the competitive inhibition of the elimination of insulin and amylin-beta. It is the insulin-degrading enzyme, which is the limiting factor. This involves simple dietary changes where the patient cuts out sugar and limits starchy foods in the diet. This normalizes insulin levels and the IDE function returns to normal.
  3. Alzheimer’s patients and patients with mild cognitive dysfunction should be tested with glucose tolerance tests (GTT). It the test is abnormal, a knowledgeable dietician should be consulted.
  4. Obesity is strongly associated with hyperinsulinemia and diabetes. Again frequent GTT should be done followed by dietary intervention when abnormal.
  5. Professor Melissa Schilling stated that 86 million Americans are pre-diabetic, but they have no symptoms. Only glucose tolerance testing can diagnose that condition. This will prevent a lot of cases of diabetes and Alzheimer’s disease.
  6. Large parts of the population have no knowledge of the glycemic index of carbohydrates. In order to limit glucose overload and excessive insulin production there is a need for educational nutritional programs. This will be a powerful tool in Alzheimer’s disease prevention.
High Insulin Levels Can Cause Alzheimer’s

High Insulin Levels Can Cause Alzheimer’s

Conclusion

It has been general knowledge for some time that diabetics have a higher rate of Alzheimer’s disease. People have known Alzheimer’s as “Diabetes of the brain” or “Type 3 Diabetes”. This new research has shed some light on the connection of elevated insulin to Alzheimer’s disease. It was news to me that there is a competitive inhibition of the elimination of insulin and amylin-beta via the insulin-degrading enzyme. It boils down to recognizing that sugar overconsumption causes Alzheimer’s disease. If you want to keep your brain power until a ripe old age, you better eliminate a lot of sugar and adopt a healthy Mediterranean diet.

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Oct
08
2016

Vitamin D3 Protects Your Brain

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

Vitamin D3 protects your brain from multiple sclerosis (MS)

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

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

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

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

Progression and disability in MS patients with various vitamin D3 levels

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

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

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

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

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

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

Vitamin D3 protects your brain from Parkinson’s disease

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

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

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

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

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

Vitamin D3 protects your brain from Alzheimer’s disease

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

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

What does vitamin D3 have to do with this?

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

Specifically, the researchers found the following observations.

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

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

Vitamin D3 combined with metformin suppresses cancer

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

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

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

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

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

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

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

Vitamin D3 Protects Your Brain

Vitamin D3 Protects Your Brain

Conclusion

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

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

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

Apr
23
2016

Healing Powers Of Green Tea

Powerful catechins that are a special form of bioflavonoids provide the healing powers of green tea. Researchers have proven that these catechins are only in green tea, not so much in black tea. The most effective of several catechins contained in green tea is EGCG, which stands for EpiGalloCatechin-3-Gallate. It crosses the blood/brain barrier and is very important for the protection of the brain from Alzheimer’s disease. But green tea or green tea extract has a diversified pharmacological action. Researchers said that green tea protects you from cardiovascular disease, from obesity, from diabetes, from autoimmune disorders, from cancer, from Alzheimer’s and dementia.

In the following I like to comment on how green tea or its extract can protect from all of these diseases.

Alzheimer’s disease

Although there are 5 or 6 approved anti-Alzheimer’s drugs, none of them work for very long. They may at best postpone the deteriorating memory for 6 months, but then the effect of the drug wears off. The reason is that the drugs do not stop the production of the deadly beta-amyloid. It is the beta-amyloid that damages nerve cells that you want to preserve so you can think and memorize. In contrast a simple phytochemical, the catechin EGCG has been shown in animal experiments and in human trials to stop beta-amyloid production and increase solubility of beta-amyloid fragments in the brain. The end result is better memory and no further deterioration.

Two studies showing less strokes and better working memory processing with green tea

In a study of 13,988 elderly Japanese observed over 3 years the group that consumed 3 to 4 cups of green tea daily had 33% less strokes, cognitive impairment and osteoporosis.

Researchers at the University of Basel, Switzerland enrolled 12 healthy volunteers aged 21 to 28 and fed them extracts of green tea or placebo fluid via feeding tubes. They did this to rule out taste as a factor. The patients underwent functional MRI scans and they also received memory-stimulating tasks. Only the green tea extract was boosting activity in the frontal brain of the subjects. This was located in a specific area, called dorsolateral prefrontal cortex. This area has a connection with language comprehension, reasoning and learning. It also switches short-term memory into long-term memory, called working memory processing.

Healing powers of green tea through new nerve cell development

Researchers showed with animal experiments that green tea extract protects nerve cells from the toxic effect of beta-amyloid. At the same time green tea extract triggers the production of new brain nerve cells (neurons). This is really good news for Alzheimer’s disease patients and their families: green tea extract delays further memory deterioration and stimulates the development of new nerve cells in the brain!

Cardiovascular disease

In a 2006 Japanese study 40,530 Japanese adults aged 40 to 79 years without history of stroke, coronary heart disease, or cancer at baseline were observed for 7 years. Diaries were kept about how many cups of green tea each person was drinking per day. The prevention of heart attacks and strokes was the the biggest effect of green tea extracts.

Men had a mortality reduction of 12% for heart attacks when they drank 5 cups or more of green tea; in women the corresponding mortality reduction for heart attack was 31%, a bigger effect. Overall mortality from strokes was lower than from heart attacks. This made the effect of green tea consumption even more beneficial with respect to stroke prevention. This study did not show any cancer prevention effect for green tea.

Obesity

It appears that green tea increases heat production and burns fat in the process. There was a small effect in terms of weight loss and a beneficial effect increasing the protective HDL cholesterol in this 2012 Polish study on obese patients. The authors compared either 379 mg of green tea extract, or a placebo, daily for 3 months. They concluded: “The results of this study confirm the beneficial effects of green tea extract supplementation on body mass index, lipid profile, and total antioxidant status in patients with obesity.”

Diabetes

Although there are claims in some studies that green tea would prevent diabetes, this question was thoroughly investigated in this Chinese 2014 study.

Researchers did not see any effects on fasting blood sugars or on hemoglobin A1C values. Hemoglobin A1C is a very sensitive indicator for the presence or absence of diabetes. All these lab tests showed no change following consumption of green tea or green tea extract. Forget using green tea for diabetes prevention; cut out sugar and starchy foods instead.

Autoimmune disorders

Sjogren’s syndrome and lupus are both autoimmune diseases. Green tea extract has shown in humans that symptom severity can improve; green tea polyphenols (GTPs) possess anti-inflammatory properties that benefit patients with autoimmune diseases.

In an animal model arthritis researchers determined that T helper cells are weakened and bone resorption is inhibited by EGCG from green tea extract.

Researchers at Harvard Medical School, Boston, MA have noted that green tea extract is useful in calming down the immune response in autoimmune diseases. They concluded: “Altogether, these studies identify and support the use of EGCG as a potential therapeutic agent in preventing and ameliorating T cell-mediated autoimmune diseases.”

Cancer

Many researchers found that EGCG from green tea extract has immune modulatory effects. Furthermore, they saw a positive effect when patients received EGCG in combination with chemotherapy. A combination of cisplatin therapy with green tea extract has been found to have more effects on colorectal cancer and ovarian cancer than each one on its own. Similarly chemotherapy of breast cancer had better results in humans when EGCG from green tea extract was added as an immune modulation. More research, particularly in humans is needed to fully understand the mechanism of action of EGCG.

Toxicity of green tea extract

Animal experiments showed that higher doses of green tea extract could cause toxicity in the liver and in the nose of rats and mice. I was not able to find objective evidence for green tea toxicity in the PubMed system with respect to humans.

Healing Powers Of Green Tea

Healing Powers Of Green Tea

Conclusion

Perhaps the most important discovery regarding green tea extract is as follows. It crosses easily through the blood/brain barrier into the brain. This can postpone Alzheimer’s disease and can even lead to new neuron formation. The beneficial cardiovascular effects are also useful and combine well with exercise and good nutrition for prevention. Particularly stroke prevention is a useful property of EGCG from green tea extract. The effect on obesity is marginal whereas there was no effect of green tea on prevention of diabetes. The immune modulatory effect of green tea extract is useful in the treatment of autoimmune diseases and of cancer. Existing treatments for these conditions are becoming more effective by adding green tea extract.

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