Once people come into their seventies, one in five will suffer from cognitive impairment. Then after five years, half of those affected with cognitive impairment will develop dementia sadly, pass away. Therefore, the sooner this process can be treated, by slowing it or stopping it, the better.
Even though an effective cure for Alzheimer’s disease is unavailable, medications just to regulate the risk factors could avoid millions of cases. A lot of effort has been spent on categorizing the risk factors associated with Alzheimer’s and developing treatments to decrease them.
There was a small study conducted in 1990 on Alzheimer’s patients, which reported high concentrations of homocysteine in their blood. The homocysteine story dates back to the 1969s, when a Harvard pathologist stated two cases of children, one from the 1933s, whose brains had turned to mush. Both cases suffered from tremendously rare genetic mutations that steered to unusually high levels of homocysteine in their bodies. The doctor then asked if homocysteine could reason for the brain damage even in people without genetic defects.
Today, homocysteine is seen as “a strong, independent risk factor for the development of dementia and Alzheimer’s disease.” A blood level count of over 14 (µmol/L) may double your risk. Then again focusing on the Framingham study, the researchers appraisal was that as many as one in six Alzheimer’s cases may be attributable to raised homocysteine in the blood, which is now thought to play a part in brain damage and cognitive and memory decay. Since our body can detoxify homocysteine, using three vitamins: folate, vitamin B12, as well as vitamin B6. But as there are studies that find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer’s disease – a cause-and-effect role can only be established by interventional studies.
Firstly, the results were inacceptable. Vitamin supplementation did not appear to work, but the studies were following neuropsychological assessments, which are more idiosyncratic compared to structural neuroimaging. That meaning that what was really happening to the brain.
Then again, a double-blind randomized controlled study concluded that homocysteine-lowering by B vitamins can slow the rate of speed that the brain was deteriorating in individuals with mild cognitive impairment. More so, as people age, the brain slowly deteriorating process, but the shrinking is much accelerated in indivuals with Alzheimer’s disease. An in-between rate of shrinkage is found in people with mild cognitive impairment. The reasoning was if the professionals was able to slow the rate of brain loss, then it could also mean that they would be able to slow the conversion to Alzheimer’s disease. Researchers then tried providing individuals B vitamins for a period of two years. The results was that it markedly slowed the speed of brain shrinkage. The rate of atrophy in those with extraordinary homocysteine levels was in fact also cut in half. This ended up being a rather simple and safe treatment can slow the speed which brain loss took place.
In addition, in a follow-up study added more weight by demonstrating that B-vitamin treatment lessened, by as much as seven times, the brain atrophy in the areas especially susceptible to the Alzheimer’s disease process.
Therefore, the value of the impact of B vitamins was confined to those with high homocysteine, showing a relative deficiency in one of those three vitamins. But, the question now would be if it might not be better to become deficient in the first place? Most individuals receive enough vitamin B6 and vitamin B12. The intention these people were stuck at a homocysteine of 11 µmoles per liter is that they probably were not getting sufficient amounts of folate. Folate is found concentrated in greens and beans. Ninety six percent of people in America do not even make the minimum suggested quantity of dark green leafy vegetables, never mind the recommend amount of beans.
If people were on a plant based diet, their homocysteine levels would decrease by 20% in seven days, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed quick and noteworthy homocysteine lowering without any medication or supplements suggests that multiple mechanisms may have been at work. The researchers advise it may be because of the fiber. Every gram of daily fiber eaten may rise the folate levels in the blood nearly two percent, perhaps by increasing vitamin production in the colon by all our good gut bacteria. It also could be from the lessen methionine consumption.
Methionine is where homocysteine originates from. Homocysteine is a breakdown product of methionine. This comes mostly from animal protein. If we give people eggs and bacon for breakfast and then for dinner a steak, we can get spikes of homocysteine levels in the blood. Consequently, reduced methionine consumption of plant-based diet may be an additional factor leading to lower, safer homocysteine levels.
What has been found is that people on a eat plant-based diets long-term, will have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. The question would be why? The vegetarians and vegans were getting additional folate and fiber, but not ample amounts of vitamin B12. Most vegans were at risk for developing hyperhomocysteinaemia. Meaning having too much homocysteine in their blood. This since most vegans in the study were not accompanying their diet with vitamin B12 or eating vitamin B12-fortified foods in the first place. This is vital for any person consuming a plant-based diet. If you take vegans and give these people B12, as their homocysteine levels can decrease well below 5. Still, then again why not down to 11? The answer is that meat-eaters were stuck up at 11 is seemingly because they were not getting sufficient amounts of folate. Once vegans got adequate amounts of vitamin B12, they could finally fully exploit the benefits of their plant-based diets and come out with the weak levels of all.