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


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.


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


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.


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 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


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!

Incoming search terms:


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


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.

Incoming search terms:


High Insulin Levels Can Cause Alzheimer’s

Research published in April 2016 shows that high insulin levels can cause Alzheimer’s. Alzheimer’s disease has been known to occur more often in diabetics. But until recently it was not known why there would be this association. New research from New York University (NYU) has shed light on this puzzle. 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. 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 are made up of amyloid-beta substance and of neurofibrillary tangles. This protein material is like glue, which prevents the neurons from working properly and 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, this enzyme system is overwhelmed. Amyloid-beta gets supersaturated, as it is not eliminated at a normal speed. This leads to the glue-like deposits of amyloid-beta in Alzheimer’s brains.

It is estimated that in 2004 the direct cost to the US of Alzheimer’s disease was $214 billion. By 2050 this could go up to $1.5 trillion, if no cure is found.

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. 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 are deposited.
  2. IDE requires zinc as a co-factor to work properly in breaking down amyloid-beta. Zinc deficiency is quite common, particularly in older people. With this mechanism insulin levels are normal, but amyloid-beta is removed poorly, as IDE function is diminished.
  3. 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. 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?

Several implications follow from the four mechanisms that were described above.

  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 injected insulin 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. Simple dietary changes are needed where sugar is cut out and starchy foods are limited. 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 educational nutritional programs are needed. 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


It has been known for some time that diabetics have a higher rate of Alzheimer’s disease. Alzheimer’s has also been called “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.

Incoming search terms:


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. 1008 patients were included 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 following observations were made.

  • 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. What the patients need can be easily determined 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


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 many cancers are suppressed by taking vitamin D3 regularly.

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. If your body is deprived of this valuable vitamin, the high risk of degenerative diseases will be the consequence.

Incoming search terms:


Drugs Can Cause Dementia

An April 2016 study from Indiana University found that drugs can cause dementia. There were 451 people enrolled in the study with an average age of 73. 60 of them were taking at least one or more anticholinergic drugs. Anticholinergic drugs are drugs that inhibit the neurotransmitter acetylcholine in nerves or in the brain. The end result is that spasms in the stomach, bowel or bladder are relieved. Also the many over-the-counter sleep medications that may contain anticholinergic drugs help you to fall asleep easier. In the above-mentioned study researchers measured the effects that the drugs have, using different tests. They used memory and cognitive tests to check for memory loss, reasoning and judgment. PET scans were used for measuring brain metabolism. MRI scans were used to look for structural brain changes.

Results on how anticholinergic drugs can cause dementia

Memory tests and cognitive function tests showed that those taking anticholinergic drugs did worse on memory tests, verbal reasoning, problem solving and planning. The PET scan showed that glucose utilization by the brain was down in those who were taking anticholinergic drugs. The hippocampus was particularly affected with lower glucose utilization. This is the center where short-term memory is processed. It is also the area where Alzheimer’s patients have been found to have problems with early memory loss.

MRI scans showed that there were structural brain changes in the patients that were using anticholinergic drugs. Their brains had reduced brain volume (brain atrophy) and the brain cavities in the brain, called ventricles were enlarged. Overall this meant that their brains had much less brain cells when compared to controls that did not take anticholinergic drugs.

In a 2013 study from the Indiana University researchers had established that it took only 60 days of taking cholinergic drugs to cause cognitive problems. Using drugs with only weak anticholinergic side effects, it took up to 90 days before the same cognitive deterioration could be measured.

The researchers concluded that it would be wise for physicians to consider switching a patient to medication that does not include anticholinergic side effects to prevent development of dementia or Alzheimer’s disease.

Anticholinergic drugs can cause dementia

In the study above it was stated that it was the group of anticholinergic drugs that was particularly problematic. These are over-the-counter-drugs like sleep aids, antihistamines, and incontinence drugs etc. that were having anticholinergic side effects. The more of these types of drugs are taken, the more interaction can take place, leading to full-blown anticholinergic symptoms. As people age, they collect more and more symptoms and diseases. Physicians tend to treat the symptoms with various medications, so it is not unusual for an elderly person to be on 5 or 6 different drugs. If one or more of these drugs have anticholinergic side effects, this can add up and cause the kind of observations the above mentioned clinical study showed: dementia symptoms and proof that the brain metabolism has been slowed down. The brain also experiences the structural changes of dementia that I mentioned.

Possibility that herbs and drugs can cause dementia

The problem does not stop here. It is possible that over-the-counter herbs that you may innocently get in the health food store can participate in the overall metabolic interaction of anticholinergic substances. Many herbs have pharmacological substances in them that have specific helpful effects. But whenever a drug or herb has a positive effect, quite often there is an undesirable effect or side effect.

Historically Belladonna is a poisonous plant that has medicinal values. Unfortunately many Belladonna preparations are available in health food stores that are not regulated by the FDA. Belladonna has strong anticholinergic side effects that interfere with other anticholinergic side effects.

There are many other herbs that are available without prescription.

Kava-kava is an herb and a hallucinogenic that has anticholinergic properties. Keep in mind that the more you use Kava-Kava, the more your brain gets shut down. Why? The anticholinergic effect of Kava-Kava shuts down acetylcholine, the main stimulus in your brain cells to help you think.

Passionflower is an herb that sedates and is often used as a tincture to help you to fall asleep. What is perceived as a natural effect is merely the anticholinergic effect on the central nervous system.

Hops is the calming compound found in beer. It is also often used together with other sedating herbal sleeping remedies in teas.

St. John’s wort is also on the list. In smaller doses this herbal antidepressant may be useful and may have less side effects than commercial antidepressants. But there are possible side effects of dry mouth and constipation, which are the result of the anticholinergic side effect.

Skullcap is often used in tea to help a person to fall asleep. But keep in mind that the effect of helping you fall asleep comes from the anticholinergic effect of skullcap on brain cells.

All of these herbs are not any different from the medications discussed earlier, except that they are a bit weaker with regard to the anticholinergic effect.

Street drugs can cause dementia

Many street drugs are sedating and they have anticholinergic effects. It is therefore no surprise that with chronic use of street drugs drug users can come down with dementia, even at a relatively young age. Long-term use of anticholinergic drugs is associated with delirium and dementia.

Particularly benzodiazepines, meperidine (an opioid), antidepressants and many other drugs when taken together cause dementia, in part because of additive anticholinergic activity.

In an Edinburgh study from England 34 deceased patients, who were heavily using street drugs were autopsied. Their brains were compared to healthy 16-year-old non-drug users. There was nerve cell damage in the brain area involved with learning, memory and wellbeing. The pathologist found the same dementia findings that would be present in much older Alzheimer patients. We have to conclude from this that the damage was done by the anticholinergic effect of the drugs that were used as a mix in the years prior to their deaths. There can be added toxicity to nerve cells from interacting drugs and their side effects.

Drugs Can Cause Dementia

Drugs Can Cause Dementia


Whenever you have a substance that helps to get you drowsy so you can sleep better, be careful and check that it is not because of the anticholinergic effect of an herb or an over-the-counter drug. Melatonin is an exception, because this is your body’s own sleeping hormone that your body knows. Whenever anticholinergic drugs or herbs act on your brain they can over time cause an irreversible brain atrophy, which can been shown by MRI scans as in the study mentioned above. This leads to cognitive problems including memory problems. PET scans have also shown a permanent slowdown of glucose metabolism of the brain cells of the hippocampus, where short-term memory is located. Without that function you get permanent dementia. Instead of being treated symptomatically ask your physician for the cause of your symptoms and have the cause treated. You may not always get the answer you need from conventional medicine. As the next step you may want a second opinion from a naturopath to see whether there would be an alternative treatment available that does not involve anticholinergic medications. Go to the root of the problem, avoid drugs that cause damage, and keep your brain healthy and your mental capacities without cognitive deficits!

Incoming search terms: