Can Lowering Homocysteine via Vitamin B Improve Cognitive Impairment?

As we age it’s common for cognitive functions to decline due to the increased rate of brain atrophy. According to previous studies, the amino acid homocysteine increases with age and is a marker for cognitive impairment, brain atrophy and dementia. High levels of homocysteine has also been associated with cardiovascular disease.

Because plasma concentrations of homocysteine can be reduced by dietary intake of B vitamins, researchers at the University of Oxford in England set out to test whether vitamin B supplementation would slow the rate of brain atrophy in elderly participants with mild cognitive impairment.

For the randomized, double-blind experiment, researchers David Smith et al. recruited 646 participants over the age of 70 who had mild cognitive impairment. The subjects were split into two groups and were either treated over the course of 24 months with high doses of folic acid (0.8 mg/d), vitamin B12 (0.5 mg/d) and vitamin B6 (20 mg/d), while the control group was treated with placebo.

Adherence to treatment was determined by measuring plasma vitamins and counting returned tablets. MRI scans were done at the start and end of the trial on a subset of the participants to assess the rate of atrophy.

The effect of vitamin B and homocysteine levels on brain atrophy in the elderly

Of the 168 participants that took part in the MRI scan, brain atrophy was found to be 0.76% per year in the vitamin B group and 1.08% per year in the placebo group. The trial supported the notion that homocysteine levels was associated with rate of atrophy.

They found that the rate of atrophy in participants with homocysteine levels greater than 13 µmol/L was reduced by 53% for the vitamin B group. Cognitive test scores were also shown to be higher for participants with lower rate of atrophy. Based on these results, Smith, et al., conclude that increased rate of brain atrophy in elderly individuals with mild cognitive impairment can be slowed by vitamin B intake.

Since Alzheimer’s disease, the most common form of dementia, starts with mild cognitive impairment, the researchers believe additional studies should be conducted to determine whether vitamin Bs will delay development of the disease.


Can threonine-encoding alleles reduce triglyceride levels?

High levels of triglycerides and triglyceride-rich lipoproteins are significant risk factors for cardiovascular diseases. Prevention plans to lower risk include reducing dietary total and saturated fat, but since lifestyle and genetics also play significant roles in developing heart diseases, researchers at the University of Minnesota examined the genetic variations in fatty acid binding proteins and lipid metabolism. Fatty acid binding protein 2 (FABP2) relates absorption and transportation of long chain fatty acids in the intestine. At codon 54 of FABP2, a DNA variation occurs where amino acid alanine is substituted with threonine in the protein. 

This allele of threonine at codon 54 (Thr54) can transport a greater amount of fatty acids than alanine, across the intestine into the plasma. Recent studies have found that the threonine allele have higher fasting plasma triglycerides than alanine variants.

Researchers Steven McColley, Angeliki Georgopoulos, Lindsay Young, Mindy Kurzer, Bruce Redmon and Susan Raatz hypothesize that a high-fat diet would reduce triglyceride-rich lipoproteins (TRL) and the threonine-encoding allele (Thr54) would respond by changing the transportation rate. Lipoproteins are the biochemical compounds containing both proteins and lipids that help transport fat inside and outside cells. One of their main functions is to emulsify fat molecules.

The effect of threonine-encoding alleles on triglyceride-rich lipoproteins

For the crossover study, the researchers used 16 healthy postmenopausal women as participants. The participants would undergo three different 8-week isoenergetic diet treatments: high fat, low fat, and low fat plus n-3 fatty acids.

The high fat treatment consisted of a diet where 40% of energy consumed is fat, the low fat treatment consisted of a diet where 20% of energy consumed is fat, and the low-fat plus n-3 fatty acids consisted of a diet where 20% of energy consumed is fat plus 3% as omega-3 fatty acids.

The treatments were assigned in a random order with a regular diet given 6-12 weeks between conditions. Blood samples were collected throughout the process to evaluate triglyceride levels and DNA analysis.

After assessing the data, researchers McColley et al. found that carriers of the Thr54 allele had significantly lower plasma triglycerides, chylomicron triglycerides, very low density lipoprotein and chylomicron remnant triglycerides after taking part in a high-fat diet. Participants with the Ala54 allele (alanine) did not demonstrate significant changes from baseline with any of the diets.


Part 1: Eating Insects for Your Daily Amino Acids?




The big questions about eating insects include…








L-Carnitine Supplement Could Treat Heart Disease







L-carnitine treatment and heart failure study





Can Carnitine Help Enhance Exercise Performance?

Feel like your workouts aren’t going so well? Perhaps carnitine supplements may be of use to reach your fitness goals. 

The compound carnitine is synthesized from amino acids lysine and methionine. Its role is to transport fatty acids from the cytosol to the mitochondria to help break down lipids and fats in order to create metabolic energy. The majority of carnitine is found in skeletal muscle, helping maintain co-enzyme A by creating acetylcarnitine during high intensity exercise.

In a study done by Maastricht University in the Netherlands, researchers Benjamin Wall, Francis Stephens, Dumitru Constantin-Teodosiu, Kanagaraj Marimuthu, Ian Macdonald and Paul Greenhaff hypothesized that chronic ingestion of L-carnitine and carbohydrates would increase skeletal muscle total carnitine content in healthy participants, generating various positive metabolic effects of muscle carnitine loading that would lead to an improvement in high intensity exercise performance.

For the double-blind experiment, 14 healthy, athletic male participants were used. Two weeks before the start of the trial, the participants were pre-tested for maximal oxygen consumption so individual exercises could be determined to use 50% and 80% of their maximal oxygen uptake.

For the trial phase, the subjects were to undergo the experimental protocol on three occasions, 12 weeks apart. Blood samples were collected to assess blood glucose, serum insulin and plasma total cholesterol concentration. The participants exercised for 30 mins on a cycle ergometer at 50% maximal oxygen intensity, followed by 30 mins of exercise at 80% maximal oxygen consumption. Immediately after the exercises, the participants performed a 30-min work output performance test to measure endurance and performance.

After the first experimental visit, the participants were randomly assigned to two treatment groups. The control group consumed 700 mL of a beverage containing 80 grams of carbohydrate polymer twice daily for 168 days.

The experimental group consumed the same amount of beverage but with an additional 2 grams of L-carnitine tartrate, at the same frequency. On every visit, the same exercise protocol was conducted as the first visit. Blood samples and muscle biopsy samples were also collected from the participants throughout.

The effect of L-carnitine on muscle total carnitine content and exercise performance

After evaluating the data, the researchers found that after 24 weeks muscle total carnitine content was 30% more in the carnitine group than the control, meaning a 21% increase from baseline.

This is the first study conducted that demonstrated muscle carnitine content can be increased by dietary intake in humans. It also showed carnitine plays a role in the fuel metabolism of skeletal muscle, dependent on intensity of exercise.

The researchers also found that work output was 35% greater for the carnitine group compared to the control, by the end of the trial. This represented a 11% increase from baseline measures. By increasing muscle total carnitine content, muscle carbohydrate use is reduced during low intensity exercise. For high intensity exercise, muscle carnitine reduces muscle anaerobic energy due to its enhanced generation of glycolytic, pyruvate dehydrogenase complex and mitochondrial flux.

Working as a combination, these metabolic effects lead to a reduced perceived effort but increased output, helping improve exercise performance.



The cells of the body can do without it because they use asparagine provided through diet. Asparagine, however, is not well transported to the brain via the blood-brain barrier,” said senior co-author of the study Dr. Jacques Michaud, who found that brain cells depend on the local synthesis of asparagine to function properly. First co-author José-Mario Capo-Chichi and colleague Grant Mitchell also made major contributions to the study.

Glutamine Deprivation May Slow Pancreatic Cancer

Tumor growth in pancreatic cancer patients may be slowed using glutamine. Glutamine is an amino acid, which is one of the building blocks of proteins. Although it is typically considered a non-essential amino acid (meaning the body may make it on its own), glutamine is technically a conditionally essential amino acid. The term “essential” means that it must be gotten through the diet, so this amino acid is—in certain circumstances—acquired via intake of food.

Glutamine, which is the most abundant amino acid in the human body, plays a role in cancer tumor growth; so depriving the cancer cells of glutamine may hold the key to slowing the spread of cancer of the pancreas, a study shows.

Study on pancreatic tumor growth and glutamine

At the Division of Genomic Stability and DNA Repair, Department of Radiation Oncology (part of the Dana-Farber Cancer Institute) in Boston, Massachusetts, a group of researchers and doctors, J Son, CA Lyssiotis, et al., have investigated just how the amino acid glutamine is involved with the KRAS-regulated metabolic pathway, which is part of the cause of tumor growth within the pancreas itself.

The researchers studied the metabolism of cancer cells and glutamine dependencies since, unlike normal cells, the cells within cancer tumors maintain their own type of metabolism. They said that “an increased use of the amino acid glutamine to fuel anabolic processes. Indeed, the spectrum of glutamine-dependent tumors and the mechanisms whereby glutamine supports cancer metabolism remain areas of active investigation.”

Because human pancreatic cells use a non-standard pathway, which identifies ductal adenocarcinoma (PDAC) cells, most cells use “glutamate dehydrogenase (GLUD1) to convert glutamine-derived glutamate.” What this means is that the PDAC cells “are strongly dependent … as glutamine deprivation or genetic inhibition of any enzyme in this pathway leads to [a] series of reactions [that] results in a pronounced suppression of PDAC growth in vitro and in vivo.”

The scientists established that because the glutamine metabolism is reprogrammed and “mediated by oncogenic KRAS, the signature genetic alteration in PDAC [represses] key metabolic enzymes in this pathway.”

With the PDAC pathway and pancreatic cells being dispensable, the glutamine in normal cells then becomes a possible new therapeutic approach in treating pancreatic tumors in humans. Hopefully more will be forthcoming on this new technique in the near future.


Lysine Deficiency in Vegans and Vegetarian Diet

Lysine is an amino acid that is very often found in deficient levels within vegetarians, and especially vegans. Lysine is found in abundance within meats and other protein foods, such as beef, turkey, pork, lamb, chicken, as well as fish and eggs. Since vegans and vegetarians do not typically consume animals or their products, the levels of lysine are sometimes dangerously low. How can this be helped?

Vegetarian foods that are highest in lysine

Although meat contains all 22 common amino acids, including lysine, it is not a product that vegetarians—and especially vegans–consume, Below are some suggestions for a high-lysine diet and the kind of protein foods that can provide this important amino acid.

Lysine from protein foods should include eating 1.0 to 1.1 grams/kilogram of body weight daily (for adults). This is especially important if you are over the age of 60. Vegetarian sources of lysine-containing foods, for the vegetarian that allows no mammals, but do allow some animal products, include these…

Ovo-vegetarians can eat eggs, which have all 22 amino acids, including plenty of lysine.

Pescetarians eat fish, which is also an excellent source, plus have heart-healthy oils for cardiovascular health.

Lacto-vegetarians eat milk / dairy products, which contain lesser amounts of this amino acid, but definitely more than vegetable sources.

Vegan foods high in lysine

There are definitely some high-lysine vegan foods that are available for people who do not eat any animal products whatsoever. Vegetable sources for lysine, which should be eaten daily, include:


Legumes include soybeans, and products of soybeans (such as tempeh, tofu, soy milk, soy protein, etc.), and beans (garbanzo, pinto, black beans, and other dry beans) and their products (refried beans, hummus, falafel), and peas (split, green peas, black-eyed, etc.).

Nine essential amino acids cannot be produced by the body, so must be taken in via food or through supplementation. Legumes and seitan—per serving—have the highest amount of lysine. In fact, the highest vegan foods also include tempeh, tofu, soy meats, lentils, and seitan.

Lysine is also found in fairly decent quantities within quinoa and pistachios.

The US RDA recommendation for lysine from proteins is about 1g/kg protein for children, and .8g/kg for people aged 18-59, and up to 1.3g/kg protein for people over 60.

Lysine, since it is an amino acid, can also be taken as a dietary supplement from the health food store or drug stores. Overall, there is no reason why one has to give up their vegan or vegetarian lifestyle just because they are deficient in this aminio acid. There are ample ways to include it via foods or supplementation into your daily regimen.


Chronic Liver Disease Shows Amino Acid-Sulphur Deficiency

Turns out that your liver can benefit from the sulphur-containing amino acids methionine and cysteine. Health benefits of amino acids such as these are excellent, but this is especially true for those with liver disease. As it turns out, those with chronic liver disease actually show a pattern of sulphur deficiency, so both cysteine and methionine may help with this.

Advanced liver disease and methionine / cysteine amino acids

In advanced or chronic liver disease, the metabolism of the sulphur-containing aminos, such as methionine and cysteine, are is impaired (no difference in the amino acid taurine, however).

In a study by P Almasio, G Bianchi, et al., at the Clinica Medica R, Università di Palermo, in Italy, the researchers published their discoveries based on 60 people who had chronic liver disease. The results show a pattern of amino acid deficiency in these patients.

10 of the subjects were used a control because they were healthy, but the other 50 patients had chronic liver disease, which was proven via biopsy.

The breakdown of their liver disease impairments

Hypermethioninemia (an extreme amount of methionine) was present in only these cases:

10 cases compensated cirrhosis
10 cases decompensated cirrhosis

Plus there were:

30 cases chronic hepatitis

The results of this clinical trial showed cysteine, a metabolite of methionine metabolism, was “markedly reduced in patients with compensated chronic liver disease, while in advanced cirrhosis its concentration was within the normal range.”

Methionine is an essential amino acid, which means you can only get it through diet, particularly protein foods such as meats (chicken, beef, pork, lamb, plus fish and eggs). Also, cysteine is a non-essential amino acid, which means the body can produce this amino acid on its own. No differences were observed (in plasma levels) for the amino acid taurine between groups.

What was observed was how sulfur-containing amino acid metabolism was deranged and “possibly located at various steps along the trans-sulphuration pathway, is also present in mild forms of chronic liver disease.”

What this means is that a key marker for those with chronic liver disease is that sulphur-containing amino acids are deficient. This can be true for people suffering from decompensated cirrhosis), or hepatitis.

The study did not explain whether supplementing intake with cysteine or methionine would affect the—chronic liver disease–patients in a positive way or not, but it is good to know that both of these amino acids are in ample amounts when associated with healthy livers, yet levels are abnormal in diseased livers.


Prevent Prostate Cancer with Three Amino Acids?


Study linking amino acids and prostate cancer prevention



Second study on prostate cancer and amino acids



