Just received a reply e-mail from Accera -- they expect to release Axona in mid-February.

Thanks, Deb. I emailed them but haven't received a response yet. Hoping this will be a help to many here.

I e-mailed MEDCO, our Medicare Advantage Plan medication provider, regarding Axona. They advised me that it will not be a covered medication.

I spoke with DH's neurologist at Duke about Axona. He was doubtful about it, I think partly due to the release statement....To be released mid-February as Medical Food. FDA "GRAS" (Generally Rates as Safe.)

Anyone else spoken to a neurologist about this?

Whitney - was he doubtful about it helping? Did he seem to be well informed as to what it is and what it's supposed to do??

whitney,

Who is the neurologist you speak of? I have friends and colleagues at Duke (one who is very well-informed on AD treatments).

We have discussed some of the disconnect between professional neurologists and info on these fora before. I am under the impression that even professional physicians and neurologists are bit slow on some of the info we discuss here. Many are too busy seeing patients to keep up with all the latest research and developments. Whereas, many members on these forums spend much of their free time during the day researching new treatments and reviewing some of the latest studies to help their LOs.

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Deb, I don't think he was so doubtful about it helping, I think it was more that he concerned about the statement "GRAS" or so it seemed to me. But I also think he might not be as well informed as he wanted to be. He said he was going to do some checking on it.

Oh, good. It seems that most (99%!) medical doctors "poo poo" anything that is not a PHARMAceutical. I guess they're just not trained any other way.

I mostly agree with you Deb. I am, however, under the impression that Axona can only be purchased with a prescription and used under a physician's care.

One of the reasons I think most physicians are primarily interested in pharmaceuticals is because you have to go to them for an appointment and get a prescription. If you don't need to go to a doctor's office to get a medication, it would seriously cut into a physician's revenue stream. Further, the degree to which big-pharma has penetrated medical education today is shocking.

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You are "spot on" Cerebral!

From Medivation:

"We did decide that we will not be allowing Axona during a Dimebon trial and patients can not have been on Axona for 30 days prior to enrollment."

Bummer - I was hoping to get my bro on Axona as soon as it comes out. Now I debate -- Dimebon or Axona!?

Debz,

Whats with this Axona. Never heard of it?

While at the neurologist Monday I learned that there is a new clinical trial going on across the country. No name yet, just a number. Take a look at www.kiokustudy.com. One of the doctors at Duke is involved with this but the nurse told us that DH would not be accepted because he had been on Namenda in a certain time span. You can, however, continue taking Aricept. It sounds promising and since the trials are spread nationwide, I hope someone will be able to get this and it will help. Wish DH could, but maybe he'll just get a script of Axona......

Joey:

"Accera, Inc., a biotechnology company delivering breakthrough therapies in central nervous system (CNS) diseases, will launch Axona(TM) in the United States for Alzheimer's disease (AD) in the first quarter of 2009.

Axona is a new first-in-class medical food product for the clinical dietary management of the metabolic processes associated with mild-to-moderate AD. Axona has been shown in randomized, placebo controlled clinical trials to safely improve cognitive function and memory in patients diagnosed with mild-to-moderate AD. It will be marketed as an adjunctive therapy to currently approved AD drugs. Axona will be administered under physician supervision and dispensed by prescription, in accordance with applicable FDA regulations.

"Accera's innovative, proprietary approach to AD targets the metabolic defects and imbalances associated with, and indeed characterizing the disease. Numerous scientific studies have confirmed a dramatic drop in glucose uptake in certain affected areas of the brain. This hypometabolism starts 10 to 20 years before any symptoms of AD appear. The decrease in metabolism may contribute to both the clinical and pathological course of the disease. Accera's research has shown that addressing these metabolic deficiencies may reduce the devastating effects of AD and help manage the disease."

DebZ, 30 days isn't very long, and Dimebon isn't even recruiting yet, is it? Why not try the Axona and see if it helps? Then you can decide whether you'd rather stick with that, or have your brother go off it and risk getting placebo in the Dimebon trial.

cerebral, maybe you go to the wrong doctor. My husband's doctors have all been just as willing to talk natural supplements and over-the-counter meds as prescription drugs, and have always been sensitive to the costs involved. So have my own. I wouldn't go to a doctor who put personal profit above providing the best care to his patient.

JAB,

Sounds like you go to a really open-minded doctor.

Perhaps with any profession, there are some good ones and bad ones. In healthcare especially, its vitally important to put the patient first.

Based on your research and my own, it looks like Axona may be one of the best new products now emerging. I am going to be especially interested in how it may be used in combination therapies.

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JAB - That's just what I've been thinking - try the Axona, if the results are positive, stick with it for a while - and hold up on the Dimebon trial.

I was going to get my bro on the B3 also - can't hurt, right??

Check the site http://www.about-axona.com/ (launched today; Feb 9th) to find prescribing information, study results and other information that may be of interest to you.

Looks like Axona is very similar to coconut milk powder. I was surprised to see that it actually becomes a milk when mixed.

This was kind of interesting on their website:

What is the main ingredient of Axona?

The main ingredient of Axona is medium-chain triglycerides (MCTs).

Seems perhaps a bit intentionally vague. If it becomes a milk when mixed with water and contains MCTs, my only thought is that it must be very close to coconut milk powder. Is this the substance that the FDA considers has having GRAS (generally regarded as safe) status? They also explicitly mention coconut oil saying that if one is sensitive to coconut oil, then they should not take Axona.

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Sinan, thanks for the link!

Cerebral, the information on the web site very specifically says Axona contains caprylic acid, and even provides the structure.

It also very clearly describes what a medical food is.

And I do believe we have discussed in depth and ad nauseum the fact that it is NOT "close to coconut milk".

Why, exactly, do you continue to try to mislead the people on this board?

JAB,

Does not both coconut oil and coconut milk both contain caprylic acid (along with MCTs)?

I strongly encourage everyone to do their own research and draw their own conclusions. I simply share what I have found and its up to each individual to either confirm or deny any statement I may have uttered.

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Yes, both of them contain small amounts of caprylic acid.

Coconut oil is ~5% caprylic acid ... and 85-90% unhealthy saturated fats that pose significant cardiovascular risks.

Coconut milk constituents depend on how the milk is made, but caprylic acid is typically ~1.5% of the calories, while the unhealthy saturated fats account for more than 16.1% of the calories.

Neither one strikes me as being an optimal source of caprylic acid.

Neither one could come anywhere close to meeting GRAS status requirements.

And neither one has been shown to be of benefit to AD patients in clinical trials. Axona has.

I am sure that we all would appreciate it if you would provide links to your sources, especially any that have been published in peer-reviewed journals. I believe others have already asked you to do that.

JAB,

I have given sources and links elsewhere. Another reasonably good introduction to coconut oil is on wikipedia at: http://en.wikipedia.org/wiki/Coconut_oil

You seemed to imply that Axona was different from coconut oil because Axona has caprylic acid, but so does coconut oil.

Here are what I see as some of the similiarities between coconut milk powder and Axona-

they both contain MCT's
they both contain caprylic acid
they both turn into milk when mixed with water

I am not sure what Axona exactly is because they do not tell us what the ingredients really are. They say that its "medium chain triglycerides" which could be any number of things. With virtually all medications, companies tell you what it is much more precisely. Aricept is donepezil and Razadyne is galantamine hydrobromide, for example.

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I was able to find the list of ingredients. Here is the list:

Caprylic Triglyceride, Potassium Caseinate (milk derived protein), Maltodextrin, Whey Protein (milk-derived), Sugar, Sunflower Oil, Dimagnesium Phosphate, Tricalcium Phosphate,
Dipotassium Phosphate, Soy Lecithin, Distilled Monoglyceride, Sodium Ascorbate (Vitamin C), Silicon Dioxide, Natural Vanilla Bean Extract, Vitamin E Acetate, Vitamin A Palmitate, Sucralose, Zinc Sulfate, Acesulfame Potassium, Pyridoxine HCl (Vitamin B6), Folic Acid, Chromium Chloride.

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Dr. Newport has been steadily compiling a list of journal articles.

Here are a few:

Scientific Articles about Ketones:

“Ketoacids? Good Medicine?” George F. Cahill, Jr., Richard L. Veech, Transactions of the American Clinical and Climatological Association, Vol. 114, 2003.

“The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism,” Richard L. Veech, Prostaglandins, Leukotrienes and Essential Fatty Acids, 70 (2004) 309-319.

“Ketones: Metabolism’s Ugly Duckling,” TB VanItallie, TH Nufert, Nutrition Reviews, Oct 2003, Vol. 61, No 10, 327-341.

“Brain Metabolism during Starvation,” OE Owen, AP Morgan, HG Kemp, JM Sullivan, MG Herrera, GF Cahill, Jr., J Clin Invest, 1967, Vol. 46, p. 1589-1595

“Ketone Bodies as a Fuel for the Brain during Starvation,” OE Owen, Biochemistry And Molecular Biology Education, 2005, Vol. 33 No. 4, p. 246–251

"Insulin, ketone bodies, and mitochondrial energy transduction," K Sato, Y Kashiwaya, et. al., including Dr. Richard Veech, Research Communications, The FASEB Journal, Vol. 9, May 1995, p. 651-658

"Brain metabolism during fasting," OE Owen, AP Morgan, HG Kemp, JM Sullivan, MG Herrera, GF Cahill Jr., J Clin Invest, 1967, Vol. 46, p. 1589-95

“Cerebral metabolic adaptation and ketone metabolism after brain injury,” ML Prins, 2008, Journal of Cerebral Blood Flow and Metabolism, Vol. 28, p. 1-16

“Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study,” T. VanItallie, C. Nonas, A Di Rocco, K Boyar, K Hyams and SB Heymsfield,


Scientific articles about a viral connection to Alzheimer’s disease and coconut oil medium chain triglycerides as potential viricidal agents:

“Herpes Simplex Virus Type 1 in Alzheimer’s Disease: The Enemy Within,” RF Itzhaki and MA Wozniak, 2008, Journal of Alzheimer’s Disease, Vol. 13, P. 393-405

“Inactivation of Enveloped Viruses and Killing of Cells by Fatty Acids and Monoglycerides,” H Thormar, CE Isaacs, HR Brown, MR Barshatsky, and T Pessolano, Antimicrobial Agents and Chemotherapy, Jan 1987, Vol. 31 No. 1, p. 27-31

“Development and Evaluation of Microbicidal Hydrogels Containing Monoglyceride as the Active Ingredient,” T Kristmunsdottir, SG Arnadottir, G Bergsson, and H Thormar, Journal of Pharmaceutical Sciences, Oct 1999, Vol. 88 No. 10, p. 1011-1015

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And which of the articles from Dr Newport's list would support exactly which of your conclusions?

Differences between Axona and coconut oil

(1) AXONA

Primary ingredients:
- C8 (caprylic)
- Emulsifiers (to improve bioavailability)
- Nutrients / constituents to minimize gastrointestinal upsets

Status:
- Medical food, FDA-approved for treating AD

Evidence of efficacy in treating AD:
- Clinical trials (double-blind, placebo-controlled) in AD patients, both patients who are taking AD meds, and those who are not. AD patients who did not carry the APOE4 allele improved throughout the clinical trials; those who did carry the allele held steady; placebo controls of with or without APOE4 declined significantly.

Potential health impact:
- Constituents all have FDA GRAS (Generally Recognized As Safe) status
- Clinical trials supported the safety as well as efficacy of Axona
- Substantial body of evidence in humans that C8 (caprylic) is a "neutral" fat with no negative effects on cardiovascular disease risk factors, including cholesterol levels/ratios.

Other notes:
- The mechanisms underlying the efficacy of Axona for treating AD are still being elucidated. Since Axona has been shown to raise blood levels of ketone bodies, it is thought that at least some of the mechanisms involved are related to ketone bodies. I have an excellent review article on the neuroprotective properties of methods that increase ketone body concentrations, by Maalouf, Rho and Mattson, if anyone is interested. It is not available via the web since it is still in press ... Dr Maalouf sent me an editor's proof. Other articles of note (I can send copies to anyone who would like them):
Henderson ST. 2008. Ketone bodies as a therapeutic for Alzheimer’s Disease. Neurotherapeutics 5:470-480.
Costantini LC, Barr LJ, Vogel JL, Henderson ST. 2008. Hypometabolism as a therapeutic target in Alzheimer's disease. BMC Neuroscience 9(Suppl 2):S16.
- C8 (caprylic) has antiviral activity. Unknown whether this has any relevance regarding the treatment of AD patients.


(2) COCONUT OIL

Primary ingredients (from Nutraceutical Sciences extra virgin certified; other virgin coconut oils have similar profiles):
- C12 (lauric) 49.0%
- C14 (myristic) 19.6%
- C16 (palmitic) 9.3%
- C8 (caprylic) 5.9%
- C10 (capric) 5.7%
- C18 polyunsaturated 5.4%
- C18 (stearic) 4.0%
- C18 monounsaturated 0.8%

Status:
- ~80-90% of coconut oil is saturated fats that are considered by the FDA to pose significant cardiovascular health risks

Evidence of efficacy in treating AD:
- Anecdotal only
- Might be expected to have some efficacy, taken in large enough amounts, since coconut oil is ~5-10% C8 (caprylic), which has been shown to be effective against AD in Axona clinical trials

Potential health impact:
- Substantial body of evidence from studies with coconut oil on humans that coconut oil poses a significant cardiovascular health risk, including raising cholesterol levels
- Substantial body of evidence from studies on humans that C12-C18 saturated fats pose significant cardiovascular disease risks via multiple mechanisms (see below)
- High cholesterol levels have been closely linked to the development of AD and the rate at which it progresses. Also, high cholesterol levels can be expected to exacerbate cardiovascular disease that is contributing to VaD (vascular dementia.)
- Anti-inflammatories are expected to be helpful in treating AD. Saturated fats can have an adverse effect on some anti-inflammatory agents. See, e.g., Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer DS. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J Am Coll Cardiol. 2006 Aug 15;48(4):715-20.
- Recent studies have showed that saturated fats can affect the immune system, which was unexpected. This is something that scientists are just beginning to understand. This is yet another reason it is inadvisable to sharply increase the saturated fat intake of AD patients by giving them large amounts of coconut oil, in my opinion.

Other notes:
- Substantial body of evidence, using biopsies of human fat (adipose) tissue samples from around the world, that C12 (lauric) is primarily processed via the lymph system and stored in fat (rather than transformed into ketone bodies for use as "fuel.")
- Certain trace constituents (e.g., antioxidants) found in vegetable oils are thought to be very beneficial to human health, and especially to AD patients. Coconut oil has, by far, the lowest amounts of any tocopherols and tocotrienols of any of the vegetable oils.
- C8 (caprylic), C10 (capric), and C12 (lauric) have antiviral activity. Unknown whether this has any relevance regarding the treatment of AD patients.

More details on the caardiovascular health risks of C12-C18 saturated fats:

- The C12-C18 saturated fats are all considered by the FDA to pose health risks, based on a huge body of evidence from epidemiological studies done on humans, many of which used coconut oil as the source of the saturated fats. For example, the Seven Countries Study found strong positive associations between death rates from coronary heart disease and average intake of lauric, myristic, palmitic, and stearic acids. (Each of these saturated fats, individually, was linked to coronary heart disease death rates.)

- The mechanisms whereby C12-C18 saturated fats pose health risks depend on the saturated fat involved.
* All four saturated fats (C12-C18) increase total blood cholesterol and LDL, promote post-prandial lipaemia, and, through their action on platelet adhesion, encourage thrombosis.
* Several studies showed that increasing the intake of C12 (lauric) was associated with a significant increase in risk of new atherosclerotic lesions.
* A recent meta-analysis of 60 controlled human trials found that C12 (lauric) had the largest cholesterol-raising effect of all four saturated fats; it raised the LDL levels the most of all four, but it decreased the ratio of total to HDL cholesterol due to an even greater increase in HDL. Both C14 (myristic) and C16 (palmitic) raised total serum cholesterol, but had little effect on the ratio due to similar increases on both total cholesterol and HDL.
* C18 (stearic) had minimal effect on total cholesterol, LDL, or HDL. However, in addition to the adverse activities it has in common with C12-C16 (above), C18 (stearic) has been shown to increase Lp(a) concentration and may activate Factor VII and impair fibrinolysis, all of which are considered to be cardiovascular disease risk factors.

Quite a post JAB!

For me, there are two particular issues of importance worth considering. The first is in regards to ketone bodies and how long they last given any treatment- whether we are talking about Axona, coconut oil, or MCT oil. Dr. Newport used a method to measure ketone bodies in her husband and found that coconut oil had a longer effect than MCT oil. It will be interesting to see how well Axona maintains ketone body levels throughout the day and how they compare to coconut oil and MCT oil.

The other issue that I am keeping an eye on is viral in nature. There appear to be properties in coconut oil and milk that fight viruses that may pertain to AD pathogenesis. My own research suggests that there may be a link between auto-immune disorders such as HIV and AD. Treatment strategies that account for this may be more efficacious.

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What does everyone think about Axona in the morning with breakfast, then supplementing with either coconut oil/MCT Fuel around suppertime??

Here is another interesting study correlating the Herpes Simplex Virus and AD that was recently posted on PubMed:

1: J Pathol. 2009 Jan;217(1):131-8. Links
Herpes simplex virus type 1 DNA is located within Alzheimer's disease amyloid plaques.

Wozniak MA, Mee AP, Itzhaki RF.
Faculty of Life Sciences, University of Manchester, UK.

The brains of Alzheimer's disease sufferers are characterized by amyloid plaques and neurofibrillary tangles. However, the cause(s) of these features and those of the disease are unknown, in sporadic cases. We previously showed that herpes simplex virus type 1 is a strong risk factor for Alzheimer's disease when in the brains of possessors of the type 4 allele of the apolipoprotein E gene (APOE-epsilon4), and that beta-amyloid, the main component of plaques, accumulates in herpes simplex virus type 1-infected cell cultures and mouse brain. The present study aimed to elucidate the relationship of the virus to plaques by determining their proximity in human brain sections. We used in situ polymerase chain reaction to detect herpes simplex virus type 1 DNA, and immunohistochemistry or thioflavin S staining to detect amyloid plaques. We discovered a striking localization of herpes simplex virus type 1 DNA within plaques: in Alzheimer's disease brains, 90% of the plaques contained the viral DNA and 72% of the DNA was associated with plaques; in aged normal brains, which contain amyloid plaques at a lower frequency, 80% of plaques contained herpes simplex virus type 1 DNA but only 24% of the viral DNA was plaque-associated (p < 0.001). We suggest that this is because in aged normal individuals, there is a lesser production and/or greater removal of beta-amyloid (Abeta), so that less of the viral DNA is seen to be associated with Abeta in the brain. Our present data, together with our finding of Abeta accumulation in herpes simplex virus type 1-infected cells and mouse brain, suggest that this virus is a major cause of amyloid plaques and hence probably a significant aetiological factor in Alzheimer's disease. They point to the usage of antiviral agents to treat the disease and possibly of vaccination to prevent it.

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DebZ,

I think its really going to depend on how well the ketone bodies can be maintained in the blood throughout the day, and as I suggested earlier, which treatment is most effective at combating some of the viral elements of AD.

Yet, I am still of the opinion that a combination therapeutic approach that perhaps includes but goes beyond glucose metabolism and ketone bodies is likely to have the most effect. We still need to account for Tau tangles, beta amyloid plaque build-up, acetylcholine deficiences, brain atrophy, inflammatory response issues, and overall brain nutrition with sufficient levels of fatty acids introduced through the diet to maintain DHA.

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I am really surprised that Axona is taken only once a day.

Dr. Newport's posts indicated that the residence time for ketone bodies is only a few hours.

Does anyone understand how Axona gets around this issue?

It seems that mainstream medicine agrees with the multi-front attack strategy, although they don't seem to even want to consider alternative treatments or existing, available supplements.

Drug Combinations Key In Treating Neurodegenerative Diseases
ScienceDaily (Feb. 10, 2009) — Combining the benefits of multiple drugs in a single pill may hold the key to treating neurodegenerative diseases, Medical College of Georgia researchers say... "We realize that with neurodegenerative diseases there will not be one magic bullet,” Dr. Buccafusco says. “Developing new therapeutics will require an attack on many different levels. But, right now, there are no FDA-approved compounds out there that are significantly disease-modifying. We’re at the point where we’re just getting to that.”

http://www.sciencedaily.com/releases/2009/01/090130182920.htm

We bought 8 bottles of MCT Fuel (got a good deal online + shipping) and were going to use it exclusively: 2 tbsp, 3x per day. But, after reading Dr. Newport's post on the subject, decided to hedge our bet and use the MCT fuel in the morning and evening. For mid day, we use 1 tbsp of coconut oil. I know there is some correlation between consuming this type of oil and cardiovascular disease, but I'm hoping that 1 tbsp per day is not excessive. Most "drugs" have risks and side effects that are probably worse than that of the EVCO.

swarfmaker,

I am still finding conflicts of thought on the impact of coconut oil on cardiovascular health. I would encourage you to do studies on PubMed and Google Scholar for more info. Some studies suggest that the antimicrobial and antiviral properties of coconut oil and milk may actually help prevent cardiovascular issues. Here are a couple additional studies on PubMed that may be of interest:

1: Ceylon Med J. 2006 Jun;51(2):47-51.Links

Coconut fats.

Amarasiri WA, Dissanayake AS.
Department of Physiology, Faculty of Medicine, University of Kelaniya, Ragama, Sri Lanka. lakmali_g@yahoo.com

In many areas of Sri Lanka the coconut tree and its products have for centuries been an integral part of life, and it has come to be called the "Tree of life". However, in the last few decades, the relationship between coconut fats and health has been the subject of much debate and misinformation. Coconut fats account for 80% of the fat intake among Sri Lankans. Around 92% of these fats are saturated fats. This has lead to the belief that coconut fats are 'bad for health', particularly in relation to ischaemic heart disease. Yet most of the saturated fats in coconut are medium chain fatty acids whose properties and metabolism are different to those of animal origin. Medium chain fatty acids do not undergo degradation and re-esterification processes and are directly used in the body to produce energy. They are not as 'bad for health' as saturated fats. There is the need to clarify issues relating to intake of coconut fats and health, more particularly for populations that still depend on coconut fats for much of their fat intake. This paper describes the metabolism of coconut fats and its potential benefits, and attempts to highlight its benefits to remove certain misconceptions regarding its use.
PMID: 17180807

1: Clin Biochem. 2004 Sep;37(9):830-5. Links

Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation.

Nevin KG, Rajamohan T.
Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram 695 581, India.

OBJECTIVES: The present study was conducted to investigate the effect of consumption of virgin coconut oil (VCO) on various lipid parameters in comparison with copra oil (CO). In addition, the preventive effect of polyphenol fraction (PF) from test oils on copper induced oxidation of LDL and carbonyl formation was also studied. DESIGN AND METHODS: After 45 days of oil feeding to Sprague-Dawley rats, several lipid parameters and lipoprotein levels were determined. PF was isolated from the oils and its effect on in vitro LDL oxidation was assessed. RESULTS: VCO obtained by wet process has a beneficial effect in lowering lipid components compared to CO. It reduced total cholesterol, triglycerides, phospholipids, LDL, and VLDL cholesterol levels and increased HDL cholesterol in serum and tissues. The PF of virgin coconut oil was also found to be capable of preventing in vitro LDL oxidation with reduced carbonyl formation. CONCLUSION: The results demonstrated the potential beneficiary effect of virgin coconut oil in lowering lipid levels in serum and tissues and LDL oxidation by physiological oxidants. This property of VCO may be attributed to the biologically active polyphenol components present in the oil.
PMID: 15329324

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I am new to this discussion group but have read comments on Axona. My mother was diagnosed with dementia two years ago and has declined very rapidly. Her neurologists indicated that her condition is from having TIA's or minny strokes which has resulted in front lobe shrinage. He has treated her with Alz medications including Aricept, Nmanda , Razadyne. Her deterioration has accelerated despite the treatments and when tested against benchmarks for people with her condition who receive no medication she is still below the norm. My question is this: Would Anoxa be potentially helpful for her condition? I am thinking that because her condition is a result of blood flow to the brain being compromised, it might potentially be helpful. Any comments?

Jeri, I would think it likely that Axona would help. But why don't you contact Accera and ask for their input? They know their medical food and the underlying science much better than we do.

Swarfmaker, if you'll look at the clinical trials that have been or are being conducted, you'll see there are quite a few looking at combinations of existing, available supplements. It is an interesting area of research.

Re the ketone bodies discussion:

(a) The "evidence" that ketone body levels produced by coconut oil remain in circulation longer than those produced by MCT oil is a short test in a single person, done without any sort of controls and, apparently, without paying attention to other parameters that could affect ketone body formation (such as other constituents in the diet). This does not strike me as being particularly sound evidence that the body will benefit from coconut oil. The results are particularly questionable when I haven't seen anything on how the samples were collected or the analyses were done. There are many different ways to get false responses when doing non-standard chemical analyses, and blood analysis for ketone bodies is not a standard, clinical test. The test that is used in the emergency room to screen patients who show signs of acute hyperglycemia or ketoacidosis will only detect toxic levels -- it is not sensitive enough for monitoring.

(b) According to her results, the levels of ketone bodies were considerably lower from the coconut oil than from the MCT oil. We do not know whether the level that was achieved would provide the same benefits as the levels achieved by Axona.

(c) One might think that the lower levels of ketone bodies might be due to the body failing to metabolize the MCTs in the coconut oil efficiently and/or the body failing to utilize them ... that is, even if the results are "accurate", they might actually show that the coconut oil is considerably worse than the MCT oil.

What has been shown to work, in double-blind, placebo-controlled clinical trials on AD patients, is Axona. Everything else is speculation and guesswork.

The Ceylon Medical Journal is an obscure little quarterly, published by the Sri Lanka Medical Association. The paper cerebral cites does not contain any original research; rather, it is a review that relies on a handful of publications. It makes the argument that, over the past 30 years, the diet of Sri Lankans has changed, with their average per capita consumption of coconuts decreasing from 130 to 110 coconuts per year. Over the same period of time, their incidence of ischaemic heart disease and cerebrovascular disease has risen "at an alarming rate", from one of the lowest in the world to now being the same as that of the developed world. Ergo, coconut oil must be good for you.

It does not provide any references for the claim that "most of the saturated fats in coconut" are medium-chain fatty acids that are process and used directly by the body for energy. As I have discussed elsewhere on this forum, there have been plenty of studies which show that the lauric and myristic acids in coconut oil are not used directly by the body for energy but are, rather, primarily turned into fat.

With regard to the Clin Biochem, this study was done on rats. I consider the many dozens of studies done on humans to be considerably more compelling. Please see my posts on the Ultimate Alzheimer's Cocktail thread for a number of excellent review articles, from high-profile, peer-reviewed journals, that summarize these studies and provide dozens upon dozens of references.

Finally, I consider speculation about any possible correlation between MCTs, viral infections, and the treatment of established Alzheimer's disease to be a red herring. We have discussed this on another thread. For one thing, preventing infection is a far different matter from treating an established disease. For another, Axona contains an MCT which has been shown to have antiviral properties. Moreover, the data from the Wozniak paper could just as easily be interpreted to mean that the virus gets "caught" in the diseased plaques, rather than that it causes them to form.

Clearly, from the data presented, the normal aged brain contains the virus. If the normal brain contains the virus, then the question arises: why wasn't AD triggered?

...By the way, Jeri, welcome to the forum!

I'm sorry to hear about your mother. My mother died of AD, and now my husband has it. It's very hard to watch someone you love suffer from dementia, I know.

If there is anything we can do to help you, please let us know. This particular forum is on medications and nutrient supplements. The Caregiver forum is very active, and there are many nice people who can offer you loads of good ideas on caregiving, financial support, etc. Please feel free to start a new thread there, introduce yourself, and tell us what you need. We're also quite good at offering a soft shoulder and a sympathetic ear, if you just need to vent.

JAB,

One of the main components of coconut oil that you seem to deride in your posts may be one of the keys to the anti-bacterial and anti-viral properties. It may be that the lauric acid is particularly important for AD (perhaps more so than caprylic acid). Coconut oil has an especially high content of lauric acid that is converted to monolaurin. Lauric acid is also a significant component of women's breast milk. The lauric acid in breast milk seems to help the burgeoning immune system fight off diseases (and may be useful for AD as well). Lauric acid also significantly increases metabolism.

Here is an interesting quote on lauric acid:

"Approximately 50% of the fatty acids in coconut fat are lauric acid. Lauric acid is a medium chain fatty acid, which has the additional beneficial function of being formed into monolaurin in the human or animal body. Monolaurin is the antiviral, antibacterial, and antiprotozoal monoglyceride used by the human or animal to destroy lipid coated viruses such as HIV, herpes, cytomegalovirus, influenza, various pathogenic bacteria including listeria monocytogenes and heliobacter pylori, and protozoa such as giardia lamblia. Some studies have also shown some antimicrobial effects of the free lauric acid."

If its the lauric acid, rather than the caprylic acid, that is especially pertinent to AD, then coconut oil may be advantageous over pure MCT Oil and/or caprylic acid formulations such as Axona.

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Its interesting to note that cinnamon oil also has an extremely high lauric acid content (approximately 80-90%).

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Axona has been shown to be effective at treating AD. In double-blind, placebo-controlled clinical trials.

It would appear that lauric acid is not the key for treating AD, since there isn't any in Axona.

And if you're going to quote something, give a reference.

Thanks for the Welcome. JAB, I am going to contact Accera and take your advice. At this point we are looking for new treatments as nothing she has tried has seemed to slow down her decline. I am somewhat familiar with nutrition and how it can be used with various disease states. Years ago I worked for Abbott Labs and sold nutritional products- Ensure , Osmolite, Glucerna, Pulmocare etc. so I find the premise of Anoxa interesting and worth a try. Thanks for your posts and I will be following them.

Just heard from Accera - Axona's release date is March 2nd.

To Jeri H,

Have they seen evidence of "mini-strokes" on CAT scans or MRIs? I think they call it "multi-infarct dementia" or "vascular dementia". If not, then you may be dealing with something else.

Accera has started a new web site for Axona, with prescribing information and ... a 20% discount coupon.

http://www.about-axona.com/

Thanks to all of you who have responded to my post. Swarfmaker: Yes in answer to your question. Although the neurologist never used the term "vascular dementia" I figured it out after watching the movie "Away from Her" My mother has lost the ability to associate words with objects, actions etc. and consequently the ability to communicate. Her primary care physician ordered the Cat scans but never said a word to us about there being any kind of problem (early stages). The same report went to the neurologist 6 -12 months later and he immediately recognized the atrophy. I'm hoping that we can find something to slow the process down.
JAB & Debz: Thanks so much for sharing your information with me. You guys are great!

Hi to all, I'm back after a brief trip and anxious to catch up on what's happening. I'm so glad to see the new website for Axona and plan to check it out. I hope it indicates this is safe to use in addition to Aricept since I'm unwilling to take DH off Aricept at this time.

Welcome, Jeri. I'm sorry about your Mother, but you'll find lots of support here.

Regarding the coconut oil case study of my husband, Steve, I thought you all might like to know that, after considerable experimentation with mixtures of MCT and coconut oil, we have settled on a regimen of 20 ml (4 teaspoons) of MCT oil plus 15 ml (3 teaspoons) of coconut oil each three times a day with meals to try to keep his levels of ketones high and constant. His ketone levels with MCT were higher and peaked at 90 minutes but were gone by 3 hours; with coconut oil, the levels were lower but peaked at 3 hours and therefore lasted longer. He received 20 ml of MCT oil and the equivalent of 35 ml of coconut oil at breakfast and at dinner so that we would have two sets of values for each dose. It is quite possible that the same quantity of ketones were produced,(a mathmetician could work it out...the area under the curve,) just followed a different pattern of availability. Regarding lauric acid, my biochemist researcher friends tell me that it hasn't been completely studied regarding how much is converted to ketones, etc. The ketone levels were not run by a local hospital lab, but rather a national lab. Steve is only one guy, of course, and he was his own control. He is APOE4 and it supposedly shouldn't have worked for him, but alas, it did. Regarding Aricept and Axona, the people in the Accera studies who were taking Alzheimer's meds overall had more improvement than those who were not taking these meds. I suspect if the neurons are able to function better because they have an energy source (ketones), that the neurotransmitters will work better also; the current Alzheimer's meds make the neurotransmitters more available.

Re ketone body analysis: the analyses, no matter who does them, are worthless if the samples are not collected properly, and/or stored and transported properly.

Plus, from a scientific viewpoint, two sets of data points is hardly compelling.

Even if the data is valid, we have no idea if it is better to have lower levels of ketone bodies that peak later ... it might actually be worse.

Certainly, it indicates that the coconut oil constituents are NOT being rapidly absorbed via the portal vein and immediately metabolized in the liver, as has been hypothesized.

And it may also indicate that the body is not able to utilize the ketone bodies as efficiently when coconut oil is present in the system.

Re the results with patients taking Axona plus conventional AD meds improving even more than patients simply taking conventional AD meds: this is GREAT news. It means that the Axona can be used along with the regular AD meds. So those of us whose ADLOs are doing well on those meds can continue to take them AND benefit from Axona, too!

Regarding the list of ingredients in Axona - it does not appear to have anything special other than MCTs in it.

I thought it was going to be a mix of multiple things to help AD?

JAB: Thank you very much, once again, for your detailed posts, which include lots of information and provide many new clues for us to research.

You had referred to three articles in your post dated February 10, 2009 07:26 AM; ("Axona" thread) on the neuroprotective properties of the methods that increase ketone body concentrations. I have found the third one (by Costantini LC, Barr LJ, Vogel JL, Henderson ST) and downloaded it. But for the other two, I need your help. I will be grateful if you could send me a copy (see my signature for my mail address) or, alternatively, if you could suggest any other way of getting these articles. Thank you.