Vitamin B1 (thiamine) and Dementia

Vitamin B1 and Dementia

The earliest and perhaps best example of an interaction between nutrition and dementia is related to thiamine (vitamin B1).

Throughout the last century, research demonstrated that thiamine deficiency is associated with neurological problems, including cognitive deficits and damage or disease that affects the brain. It happens when there’s been a change in the way your brain works or a change in your body that affects your brain. Those changes lead to an altered mental state, leaving you confused and not acting like you usually do.

Multiple similarities exist between classical thiamine deficiency and Alzheimer’s disease (AD) in that both are associated with cognitive deficits and reductions in brain glucose metabolism. Thiamine-dependent enzymes are critical components of glucose metabolism that are reduced in the brains of AD patients and by thiamine deficiency, and their decline could account for the reduction in glucose metabolism. In preclinical models, reduced thiamine can drive alzheimer’s disease-like abnormalities, including memory deficits, plaques, and hyperphosphorylation of tau. Furthermore, excess thiamine diminishes alzheimer’s disease-like pathologies.

In addition to dietary deficits, drugs, or other manipulations that interfere with thiamine absorption can cause thiamine deficiency. Elucidating the reasons why the brains of alzheimer’s disease patients are functionally thiamine deficient and determining the effects of thiamine restoration may provide critical information to help treat patients with AD.

A few thousand papers have been published with multiple permutations in treatments and duration, with the consistent conclusion that thiamine deficiency is associated with diminished memory.

Thiamine deficiency produces abnormalities that are similar to those in AD, and the results support the suggestion that increasing thiamine in the brain may be beneficial to patients with AD.

Thiamine has been implicated in neurological problems, delirium, and dementia. Even though a role for thiamine in neurological function has long been known, we have only a limited understanding of its multiple actions. The safety of thiamine and its analogues suggests that a carefully designed trial of thiamine analogues, with appropriate power, should be conducted in Alzheimers Disease patients.

Although thiamine deficiency has long been linked to memory deficits, the best way to increase the concentrations of thiamine and TPP in the brain is not well established. Thiamine administration does not lead to substantial changes in brain thiamine or TPP. On the other hand, if treatment is given early enough, thiamine does reverse deficits related to thiamine deficiency. Standard practice in the Western world is to treat delirious patients with thiamine and glucose. If only glucose is given, the brain can become damaged because of acidosis, and the results suggest that thiamine enters the brain to exert protective effects. In humans, administration of thiamine diminishes the symptoms of Wernicke–Korsakoff syndrome, and in animals, thiamine administration reverses the effects of thiamine deficiency on thiamine-dependent enzymes, behavior, and neuronal death, as long as thiamine is administered before the changes are irreversible. Nevertheless, thiamine is a relatively poor therapeutic in that after administration of exogenous thiamine, thiamine and TPP levels in blood rise slightly and do not remain high for a long time. On the other hand, other compounds, such as solbutaimine, benfotiamine, and fursultiamine, have been designed to increase thiamine 5 to 10 times higher than thiamine and maintain these high levels for hours.

The effects of benfotiamine on cognitive impairment and AD-like pathology alterations were tested in a mouse model of AD, where a chronic 8-week treatment of benfotiamine dose-dependently enhanced the spatial memory of mice in the Morris water maze test. Furthermore, benfotiamine effectively reduced both amyloid plaque numbers and phosphorylated tau levels.34 These effects were not mimicked by another lipophilic thiamine derivative, fursultiamine, although both benfotiamine and fursultiamine are effective in increasing the levels of free thiamine in the brain. Benfotiamine, but not fursultiamine, significantly elevates the phosphorylation level of glycogen synthase kinase (GSK)-3-α and -3-β, and reduces their enzymatic activities. Therefore, in animal models of AD, benfotiamine may improve cognitive function and reduce amyloid deposition via thiamine-independent mechanisms, or it may alter thiamine metabolism in a different manner than fursultiamine.

Benfotiamine has been shown to dramatically reduce plaques in the brain.34 In this study, a comparison with the effects of furusultiamine, which does not alter plaques, suggested to the authors that the effects of benfotiamine were independent of thiamine and likely occur through benfotiamine’s action on GSK. Although the data do raise this possibility, they are limited and leave room for alternative interpretations. One important limitation of the study is that thiamine levels were measured 1 hr after one injection or after ten days of daily administration, whereas the plaques and GSK activities were measured after daily administration for 8 weeks. Brain thiamine is well known to be resistant to short-term manipulation of peripheral thiamine. Thus, both benfotiamine and furusultiamine had only minimal effects on brain thiamine and no effects on TPP or TMP. However, benfotiamine was much more effective than fursultiamine in raising blood thiamine—blood thiamine was increased two to three times more by benfotiamine than by fursultiamine (0.1 to 15 as compared to 0.1 to 7), as well as after ten days (0.1 to 6 as compared to 0.1 to 12). Thus, over 8 weeks, these higher levels may have had a larger effect on brain thiamine. Also, the authors measured whole-brain thiamine. Mammillary bodies, which are very sensitive to thiamine deficiency, have ten times the concentration of thiamine than does the cortex.

Furthermore, endothelial cells are the cell type most sensitive to thiamine deficiency. Preventing these changes in endothelial cells protects against brain pathology, including neuronal loss. Benfotiamine has also been shown to benefit endothelial cells in diabetics by acting as thiamine. The authors suggested GSK as an alternative mechanism. However, dosages of benfotiamine that reduced plaques by 75% did not significantly alter GSK activity. Thus, although this paper is very important, the conclusion about the role of thiamine following benfotiamine requires further investigation.

Both thiamine and benfotiamine protect against the peripheral neuropathy that occurs in diabetes in humans. They both reduce advance glycation end products (AGEs) by activation of the non-oxidative portion of the pentose shunt. Benfotiamine is a better therapeutic than thiamine because it raises thiamine to much higher levels and for longer periods than does thiamine and may beneficially alter other processes as well. The pharamacokinetics of benfotiamine has been well studied and it is very safe in humans. These studies suggest that benfotiamine may be an effective treatment for AD and have stimulated a clinical trial of benfotiamine in AD patients, supported by both the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health (see

Role of the Synthetic B1 Vitamin on Health

Role of the Synthetic B1 Vitamin Sulbutiamine on Health

Role of the Synthetic B1 Vitamin on Health

Sulbutiamine is a thiamine derivative developed in Japan in the mid-60’s as a beriberi treatment drug. Since then, different potential applications have been described. For instance, there is some evidence that sulbutiamine can have anti-fatigue, nootropic, and antioxidant effects, which led to its use as a sport supplement (although some authors argue it is actually a masking doping strategy).

Moreover, this molecule has been proposed as a possible treatment for some microsporidial infections and even for certain types of cancer. Despite these potential effects, sulbutiamine is still a relatively unknown molecule, which justifies the present review, where we discuss its history and the existing literature on its health applications. We conclude that there is a great potential for sulbutiamine use, well beyond its first described function (to increase thiamine tissue concentration).

Indeed, new mechanisms of action have been found, mainly associated with its derivatives. Nevertheless, and although the research on sulbutiamine started 50 years ago, only a limited number of studies were conducted during this time frame. As so, methodological concerns need to be addressed and new studies are necessary, especially randomized controlled trials. Only then will the full potential of this versatile molecule be identified.

Casimir Funk – After reading an article by the Dutchman Christiaan Eijkman that indicated that persons who ate brown rice were less vulnerable to beri-beri than those who ate only the fully milled product, Funk tried to isolate the substance responsible, and he succeeded. Because that substance contained an amine group, he called it “vitamine”. It was later to be known as vitamin B3 (niacin), though he thought that it would be thiamine (vitamin B1) and described it as “anti-beri-beri-factor”. In 1911 he published his first paper in English, on dihydroxyphenylalanine.

Funk was sure that more than one substance like Vitamin B1 existed, and in his 1912 article for the Journal of State Medicine, he proposed the existence of at least four vitamins: one preventing beriberi (“antiberiberi”); one preventing scurvy (“antiscorbutic”); one preventing pellagra (“antipellagric”); and one preventing rickets (“antirachitic”). From there, Funk published a book, The Vitamines, in 1912, and later that year received a Beit Fellowship to continue his research.

Funk proposed the hypothesis that other diseases, such as rickets, pellagra, coeliac disease, and scurvy could also be cured by vitamins.

Sources and Functions of Common Vitamins and Minerals

Vitamin B1 (thiamine) Carbohydrate metabolism, supports appetite and nervous system function Whole grain cereals, legumes, beans, nuts, liver, pork
Vitamin B2 (riboflavin) Healthy skin and eyes, part of coenzymes in energy metabolism Dairy, meat, leafy greens, whole grains
Vitamin B3 (niacin) Part of coenzyme in energy metabolism, maintains healthy skin and digestive system Tuna, dairy, meat, nuts, proteins, whole grains
Vitamin B6 (pyridoxine) Protein absorption and metabolism, aids in red blood cell formation Whole grain cereals, vegetables, meats, nuts, eggs, bananas
Vitamin B12 (Cobalamin) Energy metabolism, nervous system and mental health Meat, fish, yogurt, cheese, eggs, soybeans, spinach
Vitamin D Bone and teeth growth, calcium absorption Sunlight, milk, egg, fish liver oils
Vitamin K Blood clotting cascade Green leafy vegetables, milk, liver, potatoes
Calcium Strengthens bones, teeth, muscular tissue, muscle action and nerve function, blood clotting Milk and dairy products
Chromium Glucose metabolism, increases effectiveness of insulin, fatty acid and cholesterol synthesis Salt, soy sauce, brewers yeast, whole grain cereals
Folic acid Part of coenzymes for new cell formation, prevention of neural tube defects, protein metabolism, proper brain function Leafy green vegetables, liver, fortified grain products, legumes, seeds
Iron Part of hemoglobin and myoglobin, increases resistance to stress and disease Meats, legumes, eggs, fish, beans
Magnesium Bone mineralization, enzyme action, nerve function Nuts, leafy green vegetables, seafood, whole grains
Potassium pH balance, nerve function, fluid balance, influences muscle activity Avocado, banana, yogurt, orange, leafy greens
Zinc Immune function, cell division, cell growth, carbohydrate breakdown Seafood, meat, nuts, seeds, chocolate

Benjamin Botox

So it would seem that I have figured out how to negate the effects of aging in my body. Or at least the things that made me look and feel older. Aches, pains, freckles, moles, age spots, liver spots, skin tags, etc. Even arthritis it seems. I’m so limber it’s ridiculous; almost comical. I can squat down, bow, touch my head to the ground and stand back up without using my hands, aside from balance.

I don’t think my body will ever look like a seventeen year old again, but that’s what I’m shooting for at this point. I’ve had so much success at this point that it is at least worth shooting for.

I am expecting that I will be able to approach a body that looks like an athletic twenty-five and be able to keep it there as long as I am willing.

It has not been easy, nor has not been cheap, but I am glad I have made the investment. It has been almost 3 years now and I expect that the full transition from my previous body of death to my new body of life will have taken about 42 months. Roughly January of 2021. Just three and a half years.

Eventually I will provide more details, but in simplest terms it would seem that for most if not all of my life my body has been running at a nutritional deficit. Though I am not certain I believe that I might even be genetically dependent on a few key nutrients. Specifically thiamine, riboflavin and niacin.

Below is the specific protocol that I will be on for a month to see what changes are affected. This should correct any nutrient deficiencies that can be corrected given enough time.

Maybe I should just call it Alpha-Vita Soup. Everything your body needs from A to Zinc.

Vitamin A-Retinyl Palmitate x 1

Vitamin B1-Benfotiamine[synthetic] x 1

Vitamin B1-Thiamine x 1

Vitamin B2-Riboflavin x 1

Vitamin B3-Niacin x 3

Boron x 3

Vitamin C-Ascorbic Acid x 3

Vitamin D3-Cholecalciferol x 1

Vitamin E-dl-alpha-tocopherol Acetate x 1

Vitamin K2-Menaquinone x 1

Alpha Lipoic Acid x 3

Beef Liver(Defatted/Dessicated) x 3

Nutritional Yeast x 6

Zinc Magnesium Aspartate x 3

Pleiotropy, Natural Selection, and the Evolution of Senescence

PDF: Pleiotropy, Natural Selection, and the Evolution of Senescence

In 1978, at the age of 52, the great evolutionary theorist George C. Williams began to chronicle his own senescence, recording once a year how long it took to run 1,700 metres round a track in Stony Brook, New York. Williams presented the graph of his 12 years of slowing speed at his acceptance speech for the Crafoord Prize in Bioscience that he shared with Ernst Mayr and John Maynard Smith in 1999. He later published it in The Quarterly Review of Biology, with which he was involved for 32 years. The plot encapsulated his lifelong fascination: why do we decline with age?

The Breast Microbiome: Who Knew?

I had no idea. The following are some starting points for anyone interested in better understanding what it means to properly care for and feed your microbes…8)

We may not be able to see them with the naked eye. Occasionally we can see proof of their existence. Frequently we experience effects of their metabolism as an itch or skin that is warm to touch. Maybe a lump or an ulceration. A painful toothache or yucky old pink eye. Plain and simple we live with microbes. And the growing consensus among academia and nutritionists alike is that we depend on them as much as they depend on us.

The Breast Microbiome: A Role for Probiotics in Breast Cancer Prevention

Diet Affects the Breast Microbiome In Mammals

The Breast Has Its Own Microbiome–and the Mix of Bacteria Could Prevent or Encourage Cancer

Unhealthy gut promotes spread of breast cancer Disrupting gut bacteria had profound, sustained effects, making cancer more aggressive


This is something that has peeked my curiosity. I am seeing way too many correlations with the human colon, our skin, fermentation and its metabolite melanoidins not to document this. Apparently our skin has the ability to ferment sugars.

Many topical self-tanners contain the compound dihydroxyacetone (DHA)[sugar]. Topical DHA[sugar] formulations come in lotions, gels, mousses, sprays, and wipes. DHA is a sugar molecule derived from plants that reacts chemically with the amino acids[proteins] in the stratum corneum[skin] to produce pigment when applied to the skin. This reaction is known as the “Maillard reaction,” and it does not require UVR[sun] to produce a pigment change. The resulting pigments are called melanoidins, which are similar in pigment to melanin.

Once DHA[sugar] is applied to the skin, it takes approximately two to four hours to begin the tanning[fermentation] process and can continue for 24 to 72 hours. DHA is resistant to normal water, soap, and sweat exposure. The tan will begin to fade gradually three to seven days after application result of normal skin exfoliation.

Melanoidins are brown, high molecular weight heterogeneous polymers that are formed when sugars and amino acids combine (through the Maillard reaction) at high temperatures and low water activity. Melanoidins are commonly present in foods that have undergone some form of non-enzymatic browning, such as 1. Barley malts (Vienna and Munich), 2. Bread crust, 3. Bakery products and 4. Coffee. And humans too.

KEY -|- They are also present in the wastewater of sugar refineries, necessitating treatment in order to avoid contamination around the outflow of these refineries.

The polymers make the constituting dietary sugars and fats unavailable to the normal carbohydrate and fat metabolism. Dietary melanoidins themselves produce various effects in the organism: they decrease Phase I liver enzyme activity and promote glycation in vivo, which may contribute to diabetes, reduced vascular compliance and Alzheimer’s disease.

Some of the melanoidins are metabolized by the intestinal microflora.




Bacteroides: the Good, the Bad, and the Nitty-Gritty – PDF

By Hannah M. Wexler

By a variety of measures, the species Homo sapiens is more microbial than human. Microorganisms comprise only a small, albeit significant, percentage of the body weight (between 2 and 5 pounds of live bacteria). However, in terms of cell numbers, we are about 10% human and 90% bacterial! Further, the number of genes in our microbiome may exceed the number of human genes by two orders of magnitude, making us genetically 1% human and 99% bacterial! Consequently, bacteria play a major role in bodily functions, including immunity, digestion, and protection against disease. Colonization of the human body by microorganisms occurs at the very beginning of human life, and many of these organisms become truly indigenous to the host.

The human colon has the largest population of bacteria in the body (in excess of 1011 organisms per gram of wet weight), and the majority of these organisms are anaerobes; of these, 25% are species of Bacteroides, the bacterial genus that is focus of this review. This review will summarize the current state of knowledge about Bacteroides species, the most predominant anaerobes in the gut. The aspects of these organisms that will be covered will include their role as commensal organisms (The Good); their involvement in human disease (The Bad); and information about their physiology, metabolism, and resistance mechanisms as well as a brief overview of clinical characteristics (The Nitty-Gritty).

Bacteroidetes is one of the major lineages of bacteria and arose early during the evolutionary process. Bacteroides species are anaerobic, bile-resistant, non-spore-forming, gram-negative rods. The taxonomy of Bacteroides has undergone major revisions in the last few decades (see “Taxonomy” below), but the genus is now limited to species within the Bacteroides fragilis group, which now number 20. Names of species within the Bacteroides or Parabacteroides group to date are listed in Table 1. Many of these species were isolated as single strains from human feces. The percentages of anaerobic infections that involve particular species of Bacteroides are indicated in Fig. 1 and were calculated from the Wadsworth Anaerobe Collection database, including more than 3,000 clinical specimens from which a Bacteroides species was isolated. The proportions of the most important species for the most common sites of isolation are indicated in Table 2. The numbers of B. fragilis isolates are 10- to 100-fold lower than those of other intestinal Bacteroides species, yet B. fragilis is the most frequent isolate from clinical specimens and is regarded as the most virulent Bacteroides species.

Bacteroides may be passed from mother to child during vaginal birth and thus become part of the human flora in the earliest stages of life. The bacteria maintain a complex and generally beneficial relationship with the host when retained in the gut, and their role as commensals has been extensively reviewed. A quote in a recent publication captured this attribute: “. . .with B. fragilis, as with real estate, it’s location, location, location”. When the Bacteroides organisms escape the gut, usually resulting from rupture of the genes. Third, both species exhibit multiple paralogous groups of genes, i.e., genes that seem to have derived from a common ancestral gene and have since diverged from the parent copy by mutation and selection or drift. The reasons for this seemingly inefficient use of genetic space are not completely clear, but it would seem that Bacteroides species are genetic “pack rats” that prefer to have all possibly needed versions of relevant proteins at hand and therefore will not need to rely on unpredictable mutations.

CONTINUE READING: Bacteroides: the Good, the Bad, and the Nitty-Gritty -PDF

Originally published in the American Society for Microbiology