Beta-Alanine Prevents Alzheimer's/Cancer/Heart Disease?

Beta Alanine a health food?

What’s worse: A bunch of excess sugar in the diet, or a bunch of oxidation in the body? Well we all know oxidation is pretty, right? The media has done a good enough job conveying that oxygen causes damage (think rust in your body) and that antioxidants are good because they prevent that. Okay, so back to the question. What about the sugar? It might make you fat, but how can it harm you? If you get too much of it once, it’s probably no big deal. Just like oxidation (think particularly hard workout session), if you get too much sugar once, most likely nothing will happen. But what about if it’s chronic?

Okay, so what happens if you replace the root word oxygen in oxidation with glycogen? You get something called glycation. Glycation is going on in your body all the time. It’s kinda like when your fry, sear, bbq etc. meat and the meat browns and even gets crispy in spots. That’s glycation, aka the browning, or Maillard reaction. Except that can happen in your brain, arteries, etc if you neglect your bodily systems that are there to prevent that from happening. Your body’s not quite as hot as a pan, but over time the effects really can add up.

In your body glycation is the process by which glucose combines with anything else really; it’s a very sticky substance and within your body, it sticks specifically to the proteins in your muscles, eyes, heart, arterial walls, brain, etc. Glycation of proteins is extremely important – likely just as important if not more so than oxidation. If it sticks around a while it produces what are called advanced glycated end products: AGEs. These things are really bad.

Glycation increases wear and tear in your body (another theory of aging) by damaging the protein so much so that white blood cells will grab a hold of it and kick it out the back door, literally. Then you have to produce more, putting more of a strain on your ability to repair and maintain your body.

This is not a theory, this is real and it only gets worse as you age, or as you further place strain on or weaken the systems in place to reduce bodily damage.

How can you prevent glycation? I don’t think you really can. How can you minimize the formation of AGEs? Ah, now we’re on to something.

What are some general approaches to improve health? Exercise, for starters, helps a lot. You can’t outwork a crappy diet, especially people trying to gain muscle or lose fat, right? But for health, tehe right kind of exercise strengthens your internal antioxidant system, by increasing things like glutathione for example. It also improves insulin sensitivity (so does fish oil, and even vit d, synthetic d3 or from the sun, as long as your blood DOH3 value ends up in a normal range, optimally ~60 ng/ml) and burns off extra blood sugar, aka glucose, the substance that causes glycation. Other healh promoters include high quality fish oil or krill oil (and to a lesser extent plants rich in ala like flax, chia, and hemp for example), both of which increase the omega 3 balance in your cells which among other things reduce inflammation. Other healthy diet choices like foods rich in antioxidants (superfood anyone), can dramatically improve health. Sugar (as can fish oil and other things that oxidize easily) can directly cause inflammation, so limiting excess (and maybe even consideration should be given too balancing it with antioxidants and noninflammatory substances) is key.

Okay so here’s my grand proposal - If glucose causes glycation, then why don’t we just get rid of blood sugar? Okay that’s just a joke. Not a very good one. We all know you can’t remove blood sugar.

AGEs and related compounds are implicated in Alzheimer’s, formation of arterial plaque, and cancer. Inhibiting their formation is an essential part of a health plan, anti-aging plan, or a prevention of Alzheimer’s plan.

There are certain drugs that can block AGE formation, but they require prescription and are expensive and safety is probably largely unknown. Carnosine on the other hand is safe, and is both an antioxidant and it prevents the formation of AGEs. Currently available drugs prescribed for Alzheimer’s disease do nothing to combat the damage caused by amyloid beta or oxidative stress, two key factors in the genesis of this devastating illness. Experimental studies, however, suggest that carnosine can help protect against both.

Based on the data I’ve seen, I think that beta alanine has a far greater ability thatn straight carnosine to increase intracellular muscle carnosine levels. I would imagine this includes carnosine in the brain and other tissues as well.

Oxidation is bad, but AGEs are no joke either. By protecting against both free radical-generated oxidative damage and AGE-generated cellular toxicity, carnosine, helps to counteract numerous, potentially harmful biochemical processes associated with aging. The best way to increase it is through timed release beta alanine supplements. The best strategy also involves limiting carbs in the diet. Its diverse effects offer support for the aging brain and cardiovascular system, and may help to modulate processes that contribute to cancer. In conclusion, Beta 7, surprisingly, appears to be a badass choice for its health boosting/protecting benefits.

More comprehensive reading:
http://nourishedmagazine.com.au/blog/articles/insulin-resistance-the-real-culprit-2
lef.org/magazine/mag2006/jan2006_report_carnosine_01.htm

Beta Alanine prevents Alzheimer’s,Cancer, and Heart Disease?! Great, now if only I could find something to prevent Alzheimers!

S

[quote]The Mighty Stu wrote:
Beta Alanine prevents Alzheimer’s,Cancer, and Heart Disease?! Great, now if only I could find something to prevent Alzheimers!

S[/quote]

Ive never used this before but - ‘LOL’

Stu, that cracked me up, cheers.

[quote]The Mighty Stu wrote:
Beta Alanine prevents Alzheimer’s,Cancer, and Heart Disease?! Great, now if only I could find something to prevent Alzheimers!

S[/quote]

[quote]The Mighty Stu wrote:
Beta Alanine prevents Alzheimer’s,Cancer, and Heart Disease?! Great, now if only I could find something to prevent Alzheimers!

S[/quote]

Haha. Of course I couldn’t say beta alanine prevents anything, but some studies have shown it’s as powerful, if not more so, than current anti-Alzheimer’s drugs in preventing AGEs, which are a big contributor for the disease. Obviously a healthy lifestyle can’t hurt either. Cheers.

great read, thanks for sharing that info tiger

[quote]The Mighty Stu wrote:
Beta Alanine prevents Alzheimer’s,Cancer, and Heart Disease?! Great, now if only I could find something to prevent Alzheimers!

S[/quote]

I’m not going to suck up to you, Stuart! NOT FUNNY

lmao

S

What?
What?
What?

A study looked at 135 elderly participants who were monitored for signs of Alzheimer’s disease for 10 to 15 years.

After they died, researchers conducted autopsies on their brains and those who had high blood sugar levels while they were alive also tended to have the plaques.

According to Reuters:

"Twenty-one participants, or 16 percent, developed Alzheimer’s disease before they died and plaques were found in all of their brains. But the autopsies also found plaques in other participants who had abnormally high blood sugar levels.

Plaques were found in 72 percent of people with insulin resistance and 62 percent of those with no indication of insulin resistance, the researchers wrote.

“The point is that insulin resistance may possibly accelerate plaque pathology (development),” Sasaki wrote."

Some abstracts implicating beta-alanine as a health promoting supplement:

Carnosine reacts with a glycated protein:
Oxidation and glycation induce formation of carbonyl (CO) groups in proteins, a characteristic of cellular aging. The dipeptide carnosine (beta-alanyl-L-histidine) is often found in long-lived mammalian tissues at relatively high concentrations (up to 20 mM). Previous studies show that carnosine reacts with low-molecular-weight aldehydes and ketones. We examine here the ability of carnosine to react with ovalbumin CO groups generated by treatment of the protein with methylglyoxal (MG). Incubation of MG-treated protein with carnosine accelerated a slow decline in CO groups as measured by dinitrophenylhydrazine reactivity. Incubation of [(14)C]-carnosine with MG-treated ovalbumin resulted in a radiolabeled precipitate on addition of trichloroacetic acid (TCA); this was not observed with control, untreated protein. The presence of lysine or N-(alpha)-acetylglycyl-lysine methyl ester caused a decrease in the TCA-precipitable radiolabel. Carnosine also inhibited cross-linking of the MG-treated ovalbumin to lysine and normal, untreated alpha-crystallin. We conclude that carnosine can react with protein CO groups (termed “carnosinylation”) and thereby modulate their deleterious interaction with other polypeptides. It is proposed that, should similar reactions occur intra-cellularly, then carnosine’s known “anti-aging” actions might, at least partially, be explained by the dipeptide facilitating the inactivation/removal of deleterious proteins bearing carbonyl groups.

Free Radic Biol Med 2000 May 15;28(10):1564-70


Carnosine: A Versatile Antioxidant and Antiglycating Agent
Carnosine ({beta}-alanyl-L-histidine) has recently attracted much attention as a naturally occurring antioxidant and transition-metal ion sequestering agent. It has also been shown to act as an anti-glycating agent, inhibiting the formation of advanced glycation end products (AGEs). Through its distinctive combination of antioxidant and antiglycating properties, carnosine is able to attenuate cellular oxidative stress and can inhibit the intracellular formation of reactive oxygen species and reactive nitrogen species. By controlling oxidative stress, suppressing glycation, and chelating metal ions, carnosine is able to reduce harmful sequelae such as DNA damage. AGEs are known contributors to the pathology of Alzheimer’s disease, and carnosine therefore merits serious attention as a possible therapeutic agent. http://sageke.sciencemag.org/cgi/content/abstract/2005/18/pe12

Carnosine protects against excitotoxic cell death independently of effects on reactive oxygen species.

The role of carnosine, N-acetylcarnosine and homocarnosine as scavengers of reactive oxygen species and protectors against neuronal cell death secondary to excitotoxic concentrations of kainate and N-methyl-D-aspartate was studied using acutely dissociated cerebellar granule cell neurons and flow cytometry. We find that carnosine, N-acetylcarnosine and homocarnosine at physiological concentrations are all potent in suppressing fluorescence of 2’,7’-dichlorofluorescein, which reacts with intra-cellularly generated reactive oxygen species. However, only carnosine in the same concentration range was effective in preventing apoptotic neuronal cell death, studied using a combination of the DNA binding dye, propidium iodide, and a fluorescent derivative of the phosphatidylserine-binding dye, Annexin-V. Our results indicate that carnosine and related compounds are effective scavengers of reactive oxygen species generated by activation of ionotropic glutamate receptors, but that this action does not prevent excitotoxic cell death. Some other process, which is sensitive to carnosine but not the related compounds, is a critical factor in cell death. These observations indicate that at least in this system reactive oxygen species generation is not a major contributor to excitotoxic neuronal cell death.

Neuroscience 1999;94(2):571-7


Carnosine prevents the activation of free-radical lipid oxidation during stress:
Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20 mg/kg body weight) induces depletion of lipid peroxidation (LPO) products in brain and blood serum, an increase of superoxide scavenging activity in brain and serum, decrease of cholesterol: phospholipid ratio and increase of easy oxidizable phospholipid portion in brain lipid extracts. After painful stress (footshock during two hours) LPO products are accumulated in brain and serum, cholesterol: phospholipid ratio increases and the portion of easy oxidizable phospholipids decreases. Carnosine given before stress prevents LPO activation. Effects of carnosine and stress are not additive: LPO inhibition induced by carnosine is much more in rats subjected to stress.

Biull Eksp Biol Med 1989 Feb;107(2):144-7