How to prevent Alzheimer’s disease. How to cure Alzheimer’s disease. These are certainly topics of growing interest in the world today. It’s been almost seven years since I devoted a newsletter to Alzheimer’s disease (AD). During that time, researchers have learned a great deal–most of which confirms what I proposed back then. But enough has changed that it’s worth revisiting the topic. And two new reports on Alzheimer’s disease make the timing particularly apropos.
Before we talk about how to prevent Alzheimer’s disease, we need to talk about what it is.
According to the National Institute of Aging, Alzheimer’s disease is defined as an irreversible, progressive brain disease that slowly destroys memory and thinking skills, and eventually even the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear after age 60. Estimates vary, but experts suggest that as many as 5.1 million Americans may have Alzheimer’s disease. It is the most common cause of dementia among older people. Dementia itself is defined as the loss of cognitive functioning–thinking, remembering, and reasoning–and behavioral abilities, to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for the basic activities of daily living.
The identifying pathological characteristics of Alzheimer’s brains include:
- Abnormal levels of beta-amyloid protein that form amyloid plaques.
- Tau proteins clump together inside neurons and form neurofibrillary tangles.
- Neurons are lost.
- And glial cells — which normally support, protect, or nourish nerve cells — are over-activated in Alzheimer’s.
The big question, though, is what is the trigger? If we want to learn how to prevent Alzheimer’s disease, we need to know what initiates it in the first place. Which of these four characteristics, if any, is the cause of Alzheimer’s and which are merely associated effects?
The Cost of Alzheimer’s Disease and Dementia
A study by the RAND Corporation just published in the New England Journal of Medicine estimates that the cumulative costs of caring for people with dementia currently ranges from $157 billion to as much as $215 billion annually in the United States.[fn] Michael D. Hurd, Paco Martorell, Adeline Delavande, et al. “Monetary Costs of Dementia in the United States.” The New England Journal of Medicine, v. 368, no. 14, Apr. 2013, p. 1326-1334. http://www.nejm.org/doi/full/10.1056/NEJMsa1204629#t=articleResults [/fn] If correct, this would mean that already the costs for dealing with dementia exceed the costs for heart disease and cancer combined. Even worse, the study projects that by 2040, these costs will nearly double.
“The economic burden of caring for people in the United States with dementia is large and growing larger,” said Michael Hurd, the study’s lead author and a senior economist at RAND, a nonprofit research organization. “Our findings underscore the urgency of recent federal efforts to develop a coordinated plan to address the growing impact of dementia on American society.”
The RAND study is based on findings from the Health and Retirement Study, an ongoing survey of individuals in the United States aged 51 and older that began in 1992, and is supported by the National Institute on Aging and the Social Security Administration. A subset of that study group received a detailed in-home clinical assessment for dementia as part of the Aging, Demographics, and Memory Study, a nationally representative examination of dementia in the United States.
The survey included an assessment of whether people could perform daily activities such as dressing themselves and preparing their own meals. Participants also were asked about their out-of-pocket health care expenses for services such as nursing home stays, home health care, and other medical services. Other questions asked whether they received help from others for their daily living activities. Medicare spending information was linked to medical claims for most participants.
The study estimated that 14.7 percent of Americans aged 71 or older suffered from dementia in 2010, a number somewhat lower than what has been found in other, smaller studies.
The total economic cost of dementia in 2010 was estimated to be $109 billion for care purchased, or $159 billion to $215 billion when the monetary value of informal care was included. The range of estimates reflects two different methods the researchers used to place a value on unpaid care. The per-person cost of dementia was $56,290 or $41,689 depending on methodology. Medicare paid about $11 billion of the dementia-related costs.
Researchers say that the main component of the dementia costs is for institutional and home-based long-term care rather than medical services. The costs associated with nursing home care and formal and informal home care comprise 75 percent to 84 percent of dementia costs.
“There are no signs that the costs of dementia will decrease given that the nation will have a larger number of 85-year-olds in the future than we do today,” Hurd said. “Unless there is some sort of medical breakthrough, these costs will continue to rise.”
What this fundamentally means is that Alzheimer’s is about the next generation–those now in their teens, twenties, and thirties. They’ll be the ones who have to pick up the tab for these astounding costs. They’ll have to pay for us–the current and in-the-pipeline older Americans.
You need to understand how big this burden actually is. At $56,290 per year per dementia patient — and with Americans having a 1-in-8 chance of getting dementia after the age of 65 (and a 1 in 2.5 chance after the age of 85) — the fiscal balance sheets of the future will be consumed by Alzheimer’s care giving costs. By 2040, we are talking about a half trillion dollars a year…just for care giving costs for dementia in the US alone. Extrapolate that out through the rest of the world, and the financial and societal impact is almost unimaginable.
President Obama recently inserted $100 million into his 2013 budget proposal that he just sent to Congress to fund the BRAIN Initiative to support technologies to map the brain.
Unfortunately, although the initiative itself had bipartisan support, the budget and anything in it that didn’t cut spending did not. At the moment, approval of funding for the initiative probably stands at about 60/40. If not approved, it might end up as a classic example of cutting off your nose to spite your face. Considering that we’re looking at a half trillion a year in costs by 2040 unless something changes, a one-time investment of $100 million to help cut that seems rather trivial. Embarrassingly, over in Europe, which is currently facing even tougher financial circumstances than the US, the Dutch government has announced that it will be investing approximately $260 million in research and care improvements (half provided by the Dutch Government and half from private sources) because it believes it will save them billions in future costs.[fn] “Millions earmarked for dementia as experts warn of looming disaster.” 4 April 2013. DutchNews.nl (Accessed 11 April 2013.) http://www.dutchnews.nl/news/archives/2013/04/despite_cuts_in_healthcare_spe.php [/fn] It would be nice to think that the US could at least match the Dutch investment–considering that the US GDP is 18 times that of the Dutch.
Genes linked to higher risk of Alzheimer’s
As mentioned earlier, a couple of new studies on Alzheimer’s have just been published. Let’s take a look at those and see how they might impact future developments.
Statistically, Alzheimer’s disease is “slightly” more common among African Americans than among white Americans living in the same community, but no genetic reasons have ever been identified for this statistical anomaly…until now.
In the largest study ever looking for genetic risk factors for Alzheimer’s in the African American population, researchers reported in the Journal of the American Medical Association that they had identified two genes that seem to be responsible.[fn] Reitz C, Jun G, Naj A, et al. “Variants in the atp-binding cassette transporter (abca7), apolipoprotein e ε4,and the risk of late-onset Alzheimer disease in African Americans. 2013/04/10 JAMA. 2013;309(14):1483-1492. http://jama.jamanetwork.com/data/Journals/JAMA/926784/joc130032_1483_1492.pdf [/fn] The press, as might be expected, made a big deal out of this, but there is less here than meets the eye.
Curiously, these same two genes are also associated with a higher risk of the neurodegenerative disorder among whites. But for reasons, as yet unknown, changes in these genes confer a higher risk of disease among African Americans than among whites. The study involved nearly 6,000 African American participants aged 60 or older, about 2000 of whom had Alzheimer’s. The researchers found that variants in the genes ABCA7 and ApoE increased the risk of developing Alzheimer’s by 80% and more than 100%, respectively. By comparison, ABCA7 is likely responsible for a 10% to 20% increased risk for Alzheimer’s within white populations (again, living in the same communities), and about 40% of whites with certain forms of ApoE are diagnosed with Alzheimer’s.
At first glance, these might look like significant differences between African Americans and whites in terms of Alzheimer’s, but medically speaking they are not. In fact, they are considered modest increases at most. From a medical point of view, a gene would need to increase the chances of getting a disease by well over 200 percent before it was identified as carrying a significant risk. And even more to the point, ABCA7 is not very common. About 9 of every 100 African-Americans with Alzheimer’s have the gene, compared with 6 out of 100 who did not have the disease. Statistically speaking, it means that when it comes to Alzheimer’s, this gene impacts only about 3 out of 100 more African Americans than whites. In other words, not very significant in the grand scheme of things. When looking for the cause of Alzheimer’s, we need to look elsewhere.
Nevertheless, the research points to the fact that genetics likely plays at least some role in Alzheimer’s, although at the moment, that role looks small. ABCA7’s role in the Alzheimer’s doesn’t come as a complete surprise; it is involved in producing cholesterol and lipids, and some research suggests that Alzheimer’s disease may involve aberrations in fat metabolism that are similar to those behind heart disease. More significantly, though, ABCA7 also regulates the transport of proteins, including those responsible for the production of amyloid plaque. And right now, the most likely culprit in the onset of Alzheimer’s is the build-up of sticky beta amyloid plaques in the brain.
Also released last week, were the results of a study published in the Journal of Neuroscience. Using a new genetically engineered lab rat that has the full array of brain changes associated with Alzheimer’s disease, the results of the study support the hypothesis that an increase in a beta-amyloid (Aß) plaque in the brain is the likely trigger of Alzheimer’s disease.[fn] Robert M. Cohen, Kavon Rezai-Zadeh, Terrence Town, et al. “A Transgenic Alzheimer Rat with Plaques, Tau Pathology, Behavioral Impairment, Oligomeric Aß, and Frank Neuronal Loss.” The Journal of Neuroscience, 10 April 2013, 33(15): 6245-6256. http://www.jneurosci.org/content/33/15/6245.abstract [/fn]
Plaque-forming beta-amyloid molecules are derived from a larger protein called amyloid precursor protein (APP). One hypothesis as to the cause of Alzheimer’s states that increases in beta-amyloid initiate brain degeneration. Genetic studies on familial forms of Alzheimer’s support the hypothesis by linking the disease to mutations in APP, and to presenilin 1, a protein thought to be involved in the production of beta-amyloid.
The researchers performed a variety of experiments confirming the presence of neurofibrillary tangles in brain regions most affected by Alzheimer’s (such as the hippocampus and the cingulate cortex), and those regions also happen to be involved in learning and memory. In the study, the rats lost up to about 30 to 35 percent of their neurons in the aforementioned brain regions. Not surprisingly, the rats also began to lose their ability to do mental tasks, like navigate a maze. And as the animals got older, they performed even worse, much as you would see in a human patient that would have these same mutations.
“Our results suggest that beta-amyloid can drive Alzheimer’s in a clear and progressive way,” said Dr. Terrence Town, the study’s senior author.
How to Prevent Alzheimer’s Disease
While we’re all waiting for the US Congress to pass funding to initiate the decades long research on the brain to find a cure for Alzheimer’s or for the pharmaceutical industry to come up with a side effect riddled miracle cure before then, is there anything we personally can do about Alzheimer’s–anything we personally can do to lower our chances of getting it, regardless of any genetic predisposition? The simple answer is that at this time there is no “proven” way to prevent Alzheimer’s disease. Fortunately, that simple answer is not necessarily the complete answer. If we look outside the medical community, we find that there are some things we can do, that although not proven, are nevertheless “a good bet.”
Assuming that the current leanings of the scientific community are correct, that beta amyloid is the key to Alzheimer’s–something that more and more studies keep pointing to–then the key to preventing AD lies in inhibiting the production of Aß plaque in the brain. And as it turns out, carnosine, a naturally occurring dipeptide that I first pointed to almost 20 years ago as likely inhibiting the formation of beta amyloid plaque in the brain, has received confirming support in that regard in multiple studies over the years.
First Carnosine Study
A 2007 study published in the Journal of Alzheimer’s Disease found that carnosine works to help Alzheimer’s patients through multiple pathways–although suppression of Aß toxicity is primary.[fn] Hipkiss AR. “Could carnosine or related structures suppress Alzheimer’s disease?” J Alzheimers Dis. 2007 May;11(2):229-40. http://www.ncbi.nlm.nih.gov/pubmed/17522447 [/fn]
First Carnosine Alzheimer’s Disease Pathway
I’m including a little extra detail in this first pathway as an example of how complex bio-chemical reactions in the human body are–and why it’s so difficult for researchers to identify them all.
- Glycated protein accumulates in the cerebrospinal fluid (CSF) of Alzheimer’s’ patients.
- Homocarnosine levels in human CSF dramatically decline with age.
- CSF composition and turnover is controlled by the choroid plexus which possesses a specific transporter for carnosine and homocarnosine.
- Carnosine reacts with protein carbonyls and suppresses the reactivity of glycated proteins.
- Carbonic anhydrase (CA) activity is diminished in AD patient brains. Administration of CA activators improves learning in animals.
- Carnosine is a CA activator.
Other Carnosine Alzheimer’s Disease Pathways
- Carnosine inhibits production of oxygen free-radicals, scavenges hydroxyl radicals and reactive aldehydes, and suppresses protein glycation.
- And, of course, as already discussed, carnosine suppresses amyloid-beta peptide toxicity.
In summary, according to the study, “These observations suggest that carnosine and related structures should be explored for therapeutic potential towards AD and other neurodegenerative disorders.”
Second Carnosine Study
A 2011 study restated the connection between Alzheimer’s and beta amyloid plaque but also reinforced the ultimate complexity of the pathways that lead to the disease–and again referred to the value of using carnosine supplementation to prevent and treat the disease throughout its multiple pathways of benefits.[fn] Carlo Corona,Valerio Frazzini,Elena Silvestri,et al. “Effects of Dietary Supplementation of Carnosine on Mitochondrial Dysfunction, Amyloid Pathology, and Cognitive Deficits in 3xTg-AD Mice.” PLoS One. 2011; 6(3): e17971. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058055 [/fn] As the study said, the pathogenic road map leading to Alzheimer’s disease is still not completely understood. However, a large body of studies in the last few years supports the idea that beside the classic hallmarks of the disease, namely the accumulation of Aß and neurofibrillary tangles, other factors significantly contribute to the initiation and the progression of the disease. Among them, mitochondria failure, an unbalanced neuronal redox state, and the imbalance of metals that naturally occur in the body like copper, iron, and zinc have all been reported to play an important role in exacerbating AD pathology. Given these factors, carnosine supplementation may be beneficial in the prevention and treatment of AD not only because it promotes a strong reduction in the hippocampal intraneuronal accumulation of Aß but also because its free-radical scavenging and metal chelating properties completely rescues AD and aging-related mitochondrial dysfunctions. Using L-carnosine supplementation, “We only observed a trend toward the amelioration of cognitive deficits.”
Third Carnosine Study
And finally, as we have mentioned multiple times, the aggregation of beta amyloid into fibrillar structures is a hallmark of Alzheimer’s disease. Thus, preventing the self-assembly of the Aβ peptide into such structures is an attractive therapeutic strategy. Well, a study published just last month in ChemBioChem indicates yet again that carnosine can do just that.[fn] Attanasio F, Convertino M, Magno A, Caflisch A, et al. “Carnosine Inhibits Aß42 Aggregation by Perturbing the H-Bond Network in and around the Central Hydrophobic Cluster.” Chembiochem. 2013 Mar 18;14(5):583-92. http://www.ncbi.nlm.nih.gov/pubmed/23440928 [/fn] Using both experimental techniques and atomistic simulations to investigate the influence of carnosine, the researchers found that carnosine seems to block the pathway toward toxic aggregates by upsetting the hydrogen bond network involved in fibrillogenesis–yet another pathway to Alzheimer’s disease.
The bottom line is that although not yet “proven” to prevent or treat Alzheimer’s disease, carnosine definitely looks like a good bet based on its ability to inhibit multiple pathways to the development of Alzheimer’s, but most especially based on its ability to prevent the formation of beta amyloid plaques in the brain.
Acetyl-l-carnitine and Alzheimer’s Disease
When I first developed a formula based on L-carnosine over a decade ago, I also included acetyl-l-carnitine (ALC), an amino acid that is naturally produced in the body. At the time, the purpose was not to address AD, but to complement the action of carnosine — particularly because of ALC’s ability to clean up lipofuscin, a waste product resulting from carnosine’s anti-glycation activity. But ALC also offered another benefit since it could so readily cross the blood-brain barrier and work to protect brain cells. Given that ability, it shouldn’t be much of a surprise that subsequent research would find that ALC might be beneficial in treating Alzheimer’s. And in fact, a 2011 study found that ALC might be able to do just that by virtue of its ability to reduce high levels of homocysteine in the brain. Specifically, the study suggested that high levels of homocysteine in the brain might play a role both in inducing tau protein to form into the filament tangles in the brain as well as Aβ accumulation–both of which are associated with the onset and progression of AD.[fn] Zhou P, Chen Z, Zhao N, Liu D, et al. “Acetyl-L-carnitine attenuates homocysteine-induced Alzheimer-like histopathological and behavioral abnormalities.” Rejuvenation Res. 2011 Dec;14(6):669-79. doi: 10.1089/rej.2011.1195. http://www.ncbi.nlm.nih.gov/pubmed/21978079 [/fn]
The researchers found that supplementation with ALC inhibited the formation of tau tangles and the accumulation of beta amyloid plaque in the brain, which “remarkably” improved the memory deficits associated with AD. To quote from the study, “Supplement of ALC almost abolished the homocysteine-induced tau hyperphosphorylation at multiple AD-related sites. Supplementation of ALC also suppressed the phosphorylation of ß-amyloid precursor proteins (APP), which may underlie the reduction of Aß.”
This makes regular supplementation with a formula based on L-carnosine and Acetyl-l-carnitine a really good bet at this point in our understanding of Alzheimer’s disease.
Note: recently, a study appeared in the news that implicated carnitine consumption and supplementation with heart disease. Don’t worry about it. There’s less here than meets the eye. Carnitine and Acetyl-l-carnitine are not the same thing, and the study is far from conclusive. In fact, four days after that study came out, a different study concluded that carnitine actually protects against heart disease. Go figure!
If you’re still thinking that supplementation with carnosine and ALC might not be the way to go and that you’d rather wait for the results of the President’s BRAIN initiative, you might want to rethink that. Of the paltry $100 million being proposed for the study–assuming that Congress ever approves it–only $28 million is actually being devoted to anything connected to Alzheimer’s.[fn] Office of the Press Secretary. “Fact Sheet: BRAIN Initiative” 2 April 2013. The White House. (Accessed 14 April 2013.) http://www.whitehouse.gov/the-press-office/2013/04/02/fact-sheet-brain-initiative [/fn] Specifically, that $28 million is to map out the brain’s neural networks and unravel how they interrelate in order to “truly understand how the brain operates in both healthy and diseased states.” In fact, there is no intention to even find a cure or treatment for Alzheimer’s in the BRAIN initiative — merely to lay “the groundwork for prevention and treatment of age-related neurological diseases.”
The bottom line is, that for now and the foreseeable future, you are on your own. If you’re looking to prevent Alzheimer’s disease, that means that the primary option available is to supplement daily with a formula that contains L-carnosine and Acetyl-l-carnitine. And it doesn’t hurt that this same formula is also likely to keep you looking younger and feeling younger in the process. Also, if you haven’t already done so, check out our previous report on Alzheimer’s for other steps you can take in support of L-carnosine and Acetyl-l-carnitine.
Terrible article – terrible
Terrible article – terrible advice. Listen to this people – 100 years ago alz was virtually unknown, today it is epidemic – why? because of idiot doctors telling people to avoid cholesterol. The brain is like 95% cholesterol – your brain needs cholesterol to stay healthy. Avoid cholesterol and your brain begins to disintegrate, and voila – Alzheimer disease. What you need to avoid like it was poison is hydrogenated fats, an unnatural type of fat that your body has trouble getting rid of. To have a healthy brain, eat saturated fats and foods high in cholesterol. And be aware of this – there is NO proof cholesterol causes any disease – go and try to find the proof – it does not exist!
HI. You are absolutely on the
HI. You are absolutely on the right track, warez, and furthermore, the wholesale poisoning of the people with fluoride and chlorine in the drinking water adds to the dilemma. And then there are also the psyche-brain-body aspects to think about. Today’s society, driven by greed and pseudo foods is another cause to look at.-
Because people have to keep the nose to the grindstone, they can no longer care for their aging kin, who become disowned and stuck into a ‘care facility’, where they are isolated from all that is dear to them. Nature has a way to deal with that. It is called amnesia and its purpose is to ease the emotional pain this upheaval produces, by shutting down some areas of the brain. This is meant to be for only short duration, but if the situation is not changed, then the ‘unused’ parts of the brain are removed physically, which is verified by neurosurgeons, who liken an Alzheimer brain to looking like a Swiss cheese. Therefore I say, that research is not looking comprehensively at this problem – they leave out the Psyche, as usual.
thanks for this input….I
thanks for this input….I believe also that it is a lack of cholesterol being metabolized which is the cause, in my case at least (can’t say I could label what I have as alzheimers, but I have had strokes JUST because of low cholesterol and low blood pressure) because I am having “symptoms” even though I eat plenty of high-saturated fatty foods, and know it most likely is because my liver is not properly metabolizing cholesterol, of which I doubt not I take in plenty! My cholesterol counts have always (since I first checked them about 50 years ago) been VERY abnormally low, even when I was tested right after taking a huge amount of what anyone would agree is very high cholesterol!!!! (Hydrogenated fats are not a part of our diet, as much as one is able to avoid.)
SO…do you have any thoughts, Abinico (or anyone else reading this comment), on how to raise cholesterol in my case (haven’t figured out what it is about the liver’s not metabolizing cholesterol which is causing inability to use the cholesterol I take in). My blood pressure is now normal, thanks to my merciful Lord using intake of licorice!
Yes, Alzheimer’s was indeed “virtually unknown” around the turn of the century because it was actually identified as a separate disease until 1906. Before then, it was just considered part of standard dementia—or old person disease.
As for cholesterol, you are correct in that most of the medical literature concerning cholesterol is a myth. In fact Jon Barron has written about that many times. http://www.jonbarron.org/article/cholesterol-myth. But that said, your argument that lack of cholesterol has caused the AD epidemic doesn’t match the facts on the ground. The simple truth is that despite doctors telling people to eat fewer cholesterol forming foods and dispensing statin drugs like candy, cholesterol levels have been steadily climbing for years. If your argument were correct, levels of AD would have plummeted to near zero, which is exactly the opposite of what has happened. Or as the Romans would say, “Res ipsa loquitur.” (The thing speaks for itself.) Then again, one should never let facts stand in the way of a good rant, right?
We would not disagree with
We would not disagree with your statement about inflammation. Jon Barron has indicated for years that systemic inflammation is a primary factor in the onset of many diseases. It’s one of the reasons he’s big on proteolytic enzymes—specifically because it reduces inflammation throughout the body. See: http://www.jonbarron.org/article/proteolytic-enzyme-formula
Wouldn’t it be beneficial to
Wouldn’t it be beneficial to add alpha lipoic acid or R-lipoic acid with the acetyl-L-carnitine?
Yes, you are correct, lipoic
Yes, you are correct, lipoic acid has been shown in test tube and animal studies to be protective against beta amyloid. But for now, carnosine still appears to be top of the food chain when it comes to protecting against plaque build-up in the brain.
I read somewhere that the
I read somewhere that the guilty party is TRANS FATS. I agree with abinico about cholesterol.
See our response to Albinico.
See our response to Albinico.
Extremely interesting! I
Extremely interesting! I recently started usuing carnosine along with the other two supplements you mention. I had to order the carnosine from overseas (I live in South Africa) as the chemist said it was exactly the same thing as the L-Carnotine!
I don’t know if it helps at all, but, as you said, it’s a good bet!
Albinico is EXACTLY right
Albinico is EXACTLY right with his comments on cholesterol and stable, saturated fats. Another interesting tidbit: Paleontologists believe it it was when our ancient hominid ancestors learned to use tools to break open the bones of their prey in order to get at the rich, fatty marrow and brain that they really began to evolve into the H. sapiens that we are today. Avoid manmade, plant-based, and hydrogenated fats like the plague. Eat the wholesome (and tasty!) fats that your great-grandparents enjoyed.
See our response to Albinico.
See our response to Albinico.
So what about virgin coconut
So what about virgin coconut oil?
Our bodies are designed to
Our bodies are designed to function at optimum elves at a certain ph, the same as the ground we grow our food. When the ph in our soil erodes to acidic levels the soil becomes diseased, nutrients are not absorbed and bacteria and fungus sets in. With the simple act of raising the ph in the soil by adding the mineral “lime” which causes the ph to rise to more alkaline levels, the bacteria and fungus are killed, the nutrients once again are absorbed properly and good healthy produce are raised for human consumption. Now the point is choosing the right ingredients to put in our bodies which will maintain a ph of approx 7.2, 7.3 is critical. Your blood maintains 7.365 and must to remain healthy (and keep you alive). The not so hard to understand lesson in this is eat the right balances of food which keeps your ph balance at around 7.2. Don’t get caught up in exact numbers and swallow the camel just apply good common sense measures. I am not a chemist, nor am I in the medical establishment in any way, I am a layman that believes God did not give the smarts to some to keep others in the dark for profit reasons but this is exactly why the obvious truth is not out there. It’s in all walks of life,especially in corporations with the only motivation is money. Conclusion, “Eat an alkaline diet, mostly fruits and vegetables, clean meats meaning no scavenger types, etc. Eat as close to the farm (fresh) as you can get, not out of a box with chemicals which cause all this toxicity. The best antioxidants are green vegetables first and the darker colors fall next and all others have there hidden benefits which have yet to be discovered. Eat well……….Live well.
I understood that L-carnitine
I understood that L-carnitine and acetyl L-carnitine are very different. They provide different benefits and do not function in similar ways. So how was it correct that carnosine is identical to L-carnitine?
The article does NOT say that
The article does NOT say that carnitine and carnosine are identical. In fact, it points out they were both used in the same formula for very different but complimentary reasons.
Thanks for such an in-depth
Thanks for such an in-depth look at what we do know about AD, and the “good bets” suggested.
I am struck by the indications for l-carnosine. I was diagnosed with cataracts, but, given other contraindications in my case, opted not to have the surgery. (I live far from public transportation, and would be trapped in my “beautiful gulag” without being able to drive.) In researching other avenues for treating cataracts, I ran across eyedrops that contain l-carnosine, the theory being that we have a great deal of l-carnosine in our eyes in youth, and its gradual disappearance coincides with a process called “cross-linking” of eye proteins, which eventuates in cataracts. After about 4 months of eyedrops use, my cataract diminished to the point that my vision in the affected eye improved from not being able to see the eye chart, to 20/30 corrected. (It worked on my dog’s cataract, too!)
[I realize that the l-carnosine eyedrops’ effect are “anecdotal,” i.e., not admissible because no studies have been done on them; “anecdotal” is not synonymous with “apocryphal,” however. I can read and drive again, so nyah nyah.]
This is a stretch, but — Has anyone observed a link between cataract frequency, or age at developing cataracts, and AD? [Yes, I realize there are many other factors that contribute to cataract development, and AD, too.], We can at least look.
Two months of astaxanthin 12
Two months of astaxanthin 12 mg single dose /d cleared most of my cataracts together with full Bill Henderson protocol for cancer treatment – maybe both but my money is on astaxanthin.
Purely fortuitous as my concern was / is cancer but very pleasant. Prefer the science when I can find it but very happy with anecdotal if it proves out clinically or otherwise. My heroine of all time is Dr Joanna Budwig 50 years ahead of current cancer therapies – conventional ones that is.
Baseline’s statement above
Baseline’s statement above that cholesterol levels have been steadily climbing for years begs the supply of a reason – the most logical one seems to be that levels of chronic inflammation have also been rising for years and the bodies response to that is to increase cholesterol production just as it is programmed to do. Taking care of chronic inflammation would appear to cure a huge range of health issues.