Got an email back and placed a phone call to one of the reps at Accera. They said it should be available. They guy said he spoke to Walgreens, RiteAid, and CVS and said it should be in my system. I told him I lived in New York City and said there must be a drug store somewhere where I can get this. He said, I know exactly where you are. He was able to pinpoint my location from my Cell Phone I suppose. Love technology! Kinda scary though... anyway...
So I put in the Axona script at my local CVS. They said it will be in on Monday at a cost of 103.00
I just got mine this morning in WV. No problem. Cost was $70.00. I forgot my coupon so he said to bring it in and he would still give me the discount. He said it looked like Humana had paid a little because the retail was $80 - some. I thought mine was pretty expensive but sounds like it is worse in NY. Mine was a small drug store chain and I find them cheaper than the big ones on a lot of prescriptions. There is a good bit in the packets. Roughtly 3 T. I would guess and it says to dissolve in juice or water by shaking and drink immediately. I tasted the powder and it is a mild sweet taste.
I am going to do the month and see if I can tell a difference between the MCT oil and it. If not I may go back to the MCT oil because of cost and ease of dosage. My dh already takes miralax in a cup of juice mornings and I doubt I can get him to drink two. I may move the miralax to later in the day.
brianna, I haven't forgotten you. I've been busily working away at it, but it's turned out to be rather complicated.
(1) MCT fuel is 2/3 caprylic acid (the active ingredient in Axona) and 1/3 capric acid. Caprylic acid has GRAS status. Capric acid does not, but that may just be because nobody ever applied for it.
Everything I found in my extensive lit search on the various saturated fats indicated that the way in which caprylic and capric fatty acids are processed is substantially different from the way in which the other saturated fats are processed. All studies on cardiovascular health indicate both of these are "neutral", i.e., they have no impact on cardiovascular risk factors.
When you see "saturated fat" on a nutritional information label, that is supposed to be, by definition, the combination of lauric, myristic, palmitic, and stearic. These are the four that the FDA and the American Heart Association consider to pose significant cardiovascular health risks. (However, Charlotte has pointed out that a bunch of MCT oil manufacturers are including caprylic and capric acids on the label, even though they're not required to.)
(2) There have been no clinical trials on Neurostin per se. There have been no scientific studies that have involved Neurostin, period, whether in humans, animal models, or cell/tissue cultures. I couldn't dredge up a single hit on Google Scholar, which is amazing.
(3) So now, I'm looking at the individual components. The only one I've delved into so far is Alpha-GPC.
This is where it's been getting complicated. I've waded through a gazillion abstracts and papers. So far, let's just say that I'm not wildly impressed with its potential for treating dementia.
Re: Neurostin...The components included in Neurostin are all in the supplements (from Life Extension Foundation) that my husband has been taking for a few years. I have no idea whether or not they have slowed his decline--just as I cannot say whether or not Aricept or Namenda have been helpful either. They didn't improve the situation--but they may have slowed the decline. I have no clue.
Thank you so much Sunshyne. I had no doubt that you were not checking it out and your labor is much appreciated! Our daughter was here this morning and she was impressed with her dad's "progress." He has 1 T. MCT Fuel with each meal. I'm thinking of trying the cinnamon also.
As far as Neurostin is concerned, I think when I read the statement: If you have experienced one or more of these symptoms, you should consider Neurostin. 1) Do you forget names or dates? 2) Do you sometimes get confused? 3) Do you find it difficult to do more than one thing at a time? 4) Do you often forget why you walked into certain rooms? 5) Do you find it hard to concentrate?
...I realized I need this product as much as DH!! It may be a good thing, but I'm not convinced. I want things that will improve, however, as Lori stated, if something will slow the decline that would be acceptable.
Well I took my coupon back to the pharmacy and he showed me that on the bottom of the coupon it says if Medicare is involved the coupon is no good. He said most coupons are that way so unless the AD patient is NOT on Medicare you might as well discard it. They make those things so they sound good then in the fine print void it.
brianna, if you think you need help, try the MCT Fuel.
I think I've done enough on the Alpha-GPC, and if it were my husband, I would not -- NOT NOT NOT -- give him Neurostin. Just on the basis of what I've learned about alpha-GPC, the Neurostin not only is unlikely to help, but may actually do harm.
This will be a long post, so I'm breaking it up at reasonable points.
There are many names for "Alpha-GPC", which is part of what complicated my search. Google Scholar does not look for pseudonyms, but only the exact word that is entered, and exactly as spelled. PubMed will look for all pseudonyms of a given compound, but does not search as many journals. Pseudonyms that have been used for "Alpha-GPC" include glycerophosphocholine (GPC), glycero(3)phosphocholine, glycerylphosphorylcholine, L-alpha-glycerylphosphorylcholine (Alpha-GPC), choline alfoscerate, and choline alphoscerate.
Acetylcholine is an important neurotransmitter, and its levels are lower in the brains of AD patients. The concept of "cholinergic-precursor loading", to increase the synthesis of acetylcholine, was originally proposed for treating AD more than 30 years ago. There was a flurry of clinical trials in the early 1990's, to test a number of different compounds that are involved in the acetylcholine cycle, including choline, phosphatidylcholine (lecithin), phosphatidylserine, cytidine 5'-diphosphocholine (CDP-choline, or citicoline), and GPC. Trials on choline and lecithin showed no efficacy at all. Apparently, CDP-choline showed some very modest benefit, although I did not research that compound specifically -- I focused on the GPC -- and the evidence for CDP-choline may be just as poor as for GPC.
There was a review, written in 2001 by a group in Italy, which claimed that 13 clinical trials, involving more than 4,000 patients, indicated GPC was effective. (This is apparently the basis for the claims in the neurostin.com website.) However, when you dig into the details, two thirds of the patients were involved in trials on using GPC to treat stroke, TIAs, or "acute cerebral ischemia".
Only a third of the 4,000 patients had what these authors call "dementia"; and the trials involved a variety of different dementia disorders (AD, vascular dementia, and "senile organic brain syndrome"), plus brain injuries from cardiac bypass surgery, subdural hematomas, cerebral contusions, or concussions.
Each individual "dementia" trial was very small; none lasted more than three months; and for the most part, they were "open label." The majority of patients were tested in trials that didn't involve controls (did not have any placebo-only patients for comparison). Several divided the tiny patient pool across multiple types of treatment (e.g., CDP-choline, GPC, and/or acetyl-l-carnitine, plus placebo if used). It appears that both males and females may have been included in the test groups, further complicating the issues ... and they did not control for age, or, apparently, other health issues.
By the time all the dust had settled, it turns out that only 19 patients with probable AD were tested, with half of those receiving placebo.
And on top of all that, *none* of the trials involved oral GPC. Instead, the GPC was administered by injection, either intramuscular or intravenous.
In short, there is NO evidence, whatsoever, that oral GPC might be of benefit to patients suffering from any type of cognitive dysfunction.
The cholinergic-precursor approach died a very abrupt death right around the turn of the century, which was very curious. At the very least, if the clinical trials were in the least bit promising, one might have expected larger, better-designed trials. Even the Italian group started writing papers which said the positive results seen with GPC "should be regarded with caution due to the small number of patients included in controlled clinical trials." However, they still suggested that basic concept was sound, and that the "problem" was that the right precursor had not yet been discovered. And if that's true, why aren't we looking for it?
Something must have happened, but what?
For one thing, a second approach for increasing the amount of acetylcholine in the brain had also been under study; i.e., the use of acetycholinesterase inhibitors (AChEIs), such as tacrine, aricept, exelon, and razadyne, to slow down the degradation of acetylcholine. I found a number of papers whose abstracts implied that the GPC approach was abandoned because the AChEI approach was considerably more effective than even the purported results from the tiny Italian trials.
Well, but why not combine cholinergic-precursor loading with cholinesterase inhibition, for even better efficacy?
Of considerably more interest, other authors implied that the scientific community had learned enough by this point to know that the basic cholinergic-precursor loading approach was seriously flawed. Parkinson's disease is another neurodegenerative disease that involves a decrease in a neurotransmitter -- in this case, dopamine. And studies had shown that dopamine replacement therapy, via the administration of the dopamine precursor L-DOPA, might drastically improve the course of the Parkinson's syndrome. Ergo, when the discovery was made that patients suffering from dementia were consistently found to have low levels of another neurotransmitter, acetylcholine, it was naturally expected that replacement therapy could be equally successful. Various approaches were tried, including acetylcholine precursors, AChEIs, and receptor agonists. In spite of expectations, none of these therapeutic approaches provided anything that came even remotely close to the Parkinson's therapy.
This is where I was when I posted previously, to let brianna know I was still alive and working the problem. I think it's a good thing I kept going (although this search was rapidly becoming more painful to my poor, befuddled brain than the saturated fats search.)
I couldn't pull the full papers for some of the abstracts that implied the basic concept was flawed, and the full papers for others simply made statements to that effect, without providing references. I wanted details. So I kept digging.
Researchers were making the very simplistic assumption that acetylcholine was the only factor responsible for memory and cognition; and that changing its concentrations would not affect anything BUT memory and cognition.
The one GPC study that was actually done on AD patients measured the plasma levels of four hormones at baseline and again at three months (the end of the trial) and found that GPC significantly decreased plasma cortisol and ACTH levels, while increasing growth hormone levels. Only prolactin was unaffected. (The other GPC studies didn't even bother to look for things like this.) Health food nuts tell you this means patients are being "revitalized", but what it actually tells you is that a lot of things are going on that weren't predicted from the original "cholinergic precursor loading" hypothesis. And while the GPC trials were going on, the rest of the scientific world was starting to unravel the complexities of the cholinergic system.
As one paper, published in 1997, said: "Alzheimer's dementia results from complex neuron alterations [which also affect muscarinic receptors among other (sub)cellular structures] rather than simply reflecting acetylcholine impoverishment. .... Accordingly, the conventional acetylcholine agonist-antagonist model of dementia now appears questionable, and replacement treatment with compounds enhancing acetylcholine function proved disappointing. It is suggested that (nonspecific) acetylcholine action becomes function-specific, as determined by the architecture of local brain circuits in which it is involved."
The overall mechanisms involved in the cholinergic system are extremely complex and interwoven, and involve many different enzymes, transporters, and receptors, as well as acetylcholine storage in and release from synaptic vesicles. A host of cholinergic abnormalities may contribute to cognitive dysfunction in AD, including alterations in choline transport, acetylcholine release, the expression of nicotinic and muscarinic receptors that bind acetylcholine, neurotrophin support, and perhaps axonal transport. Cholinergic abnormalities may also contribute to *noncognitive* behavioral abnormalities; contribute to the deposition of the Abeta plaques in AD; and even affect immune reactions. And, finally, in addition to the cholinergic system, other neurotransmitter systems are involved in AD (e.g. serotonergic, noradrenergic, glutamatergic, and dopaminergic), and each apparently influences the functions of the others.
To make things even more complicated, cholinergic neurons not only use choline for the synthesis of the neurotransmitter acetylcholine -- cholinergic neurons ALSO use choline for the synthesis of a key membrane constituent, phosphatidylcholine. When physiologically active, the neurons use free choline, taken from the "reservoir" in membrane phosphatidylcholine, to synthesize acetylcholine. This can lead to an actual decrease in the quantity of membrane per cell.
The brains of Alzheimer's patients contain lower amounts of choline and acetylcholine and HIGHER amounts of membrane breakdown products including glycerophosphocholine (GPC), in both the cholinergic and noncholinergic brain regions.
The AD brain already contains far more GPC -- as much as 150% more -- than a healthy brain.
So if the AD brain already has much higher amounts of GPC than the healthy brain, how can administering even *more* GPC to the AD patient be expected to help?
OK, so all of this helps explain why giving an AD patient GPC may not help in the synthesis (or storage, or release, or effectiveness) of acetylcholine ... but do we really care, other than that it might cost a bit more money to dose the patient with Neurostin?
YES, we should care -- very much.
For one thing, we are clearly monkeying around with the biochemistries of the body by administering GPC, with very little knowledge about what we might actually be affecting. Remember that even the very simple GPC clinical trial on AD patients, which only analyzed the blood for four hormones, found that three of the four apparently unrelated factors that were measured had been affected, i.e., plasma cortisol, ACTH, and growth hormone levels, within a short time of initiating GPC therapy. Who knows what might have been triggered if the imbalance was perpetuated by continuing therapy?
One review, published in 2008, said: "Recent evidence strongly demonstrates that acetylcholine (ACh) is not only involved in the function of the central and peripheral nervous systems, including the parasympathetic and somatic systems, but also acts as a ubiquitous cell signaling molecule or cytotransmitter, and as a hormone with paracrine, juxtacrine and autocrine properties. This active molecule exerts versatile and potent functions which modulate numerous biomechanisms, including cell growth, survival, proliferation and differentiation, cell-cell contact, cell cycle, locomotion, electrical activity, immune function, apoptosis, organization of the cytoskeleton, trophic functions, secretion, adhesion, resorption, and stress-response-regulation. By nature, the precise ACh levels and responses from receptors must be controlled and regulated by its degrading enzymes, the cholinesterases (ChEs) ... The mechanisms of many diseases ranging from the acute cholinergic crisis to the chronic degenerative and hypergenerative disorders such as Alzheimer's disease, cancers, atopic dermatitis, may involve a deficiency of ChEs or imbalance between ACh and ChEs, initially or consequentially..."
For example, the binding of acetylcholine to various receptors stimulates the growth of both small cell and non-small cell lung carcinomas. Increased levels of acetylcholine found in the cancers were associated with increased levels of the enzyme that synthesizes acetylcholine, and decreased levels of the enzymes that break it down. What happens if we feed GPC to a patient who is already developing lung tumors?
MORE IMPORTANTLY ... we may be monkeying around with factors that cause or accelerate the AD pathology itself.
Phospholipid abnormalities are hallmarks of the AD brain in regions, including the cortex and hippocampus, that are typically associated with the histopathological manifestations of the disease (i.e., amyloid plaques and neurofibrillary tangles). Amyloid beta (Abeta) peptides accumulate as senile plaque aggregates in human brain, and oligomers (small aggregates) of the peptides are also found in cerebrospinal fluid (CSF). Levels of glycerophosphocholine (GPC) -- which is a breakdown product of phospholipid membranes, as well as a precursor for choline -- are also sharply increased in the brain (by up to 150%) and the cerebrospinal fluid (by up to 76%) of AD patients.
Starting in the mid- to late-1990s, studies conducted using a number of techniques, including in vitro solution and membrane experiments, and NMR analyses of in vivo and postmortem brains, led several researchers to conclude that increased GPC concentrations may play a role in the deposition of the Abeta plaques observed in Alzheimer's brains, and the Abeta aggregates seen in CSF from AD patients. For example, in vitro studies on GPC and Abeta in solution and mixed with erythrocyte membranes showed that GPC changes the conformation of Abeta in solution or in membranes, enhancing its aggregation in solution, and enhancing its aggregation and accumulation in the phospholipid head-group region of membranes. Other phospholipid breakdown products do not have similar effects.
Now, this is not a totally smoking gun, but I, personally, would not be comfortable doing anything to increase the level of GPC in my husband's brain.
And I am finally satisfied that I have discovered the reasons why knowledgeable researchers stopped studying GPC as a treatment for Alzheimer's.
Charlotte-when I first told my kids about dogpile they thought I was crazy. I was the first to use Google and at that time I was wondering about myself- Sometimes I feel like a pioneer
This is very interesting - we heard about it on the radio the other day. It is made by a company in Colorado, where we live. I am going to ask my doctor about it tomorrow. Very interesting about the Alzheimer brain not processing glucose correctly. My DH's mother has blood sugar issues and takes Metformin, but he never has had any glucose problems that I am aware of. However, he CRAVES fruit and sweets - so could it be that is because the brain is starving for glucose/energy and craves the sugar?
Shannon - I take cinnamon for insulin resistance. I can tell it helps because I use to get blurred vision even when not eating a lot of sugar. As long as I take it, I am fine. My fasting blood sugars come back fine, but I have PCOS which insulin resistance is a symptom. I also give it to my hb in case there is a connection to AD.
Sunshyne, you are amazing! I hope right now you are resting after doing all that research. I hope that this will help many people (including myself) that might have thought about taking Neurostin. I've been giving DH the MCT Fuel and will continue. In fact, I received two more bottles yesterday. I don't remember if I mentioned this, but my husband was having trouble putting on his shirt before starting on the MCT Fuel. Now, he is able to do that, sometimes has to work at getting the buttons started right.....but he can do it! I'm thinking about adding cinnamon but I need to read a little more about what members are doing about amounts.... I feel as though I might have hijacked this thread and I really didn't mean to. It came about because I asked the neurologist for Axona and was turned down. I do think we have all had an opportunity to learn about another "drug" and I am eternally grateful to Sunshyne.
Actually, the thread isn't hijacked at all, brianna. This was all quite relevant to Axona. I just didn't get into that part, because I thought things were complicated enough without mentioning some of the other things I found.
On another thread, we discussed whether MCT oil or Axona might be useful for treating Parkinson's. There is a growing body of evidence suggesting that mitochondrial dysfunction and reduced bioenergetic efficiency occur in brains of patients with Parkinson's and Alzheimer's. MCT oil and Axona are believed to be effective in treating AD (and probably will be effective for Parkinson's) because the MCTs in Axona and MCT oil are metabolized into ketone bodies ... and ketone bodies are efficiently used by mitochondria for energy, and for ATP generation.
Choline is only one of the precursors needed to synthesize acetylcholine. The other is acetyl-CoA. Acetyl-CoA is synthesized from acetate and CoA; the process consumes ATP. ATP is (among many other things) a neurotransmitter, and very recent studies show that it may be taken up and stored in, and released from, synaptic vesicles, along with acetylcholine. And Alzheimer's brains synthesize less ATP than healthy brains, just as they synthesize less acetylcholine.
While looking into GPC, I also found recent studies which indicate that when cells are exposed to inhibitors of mitochondrial bioenergetics -- that is, when the bioenergetic efficiency of mitochondria is reduced -- the turnover of their major membrane phospholipid, phosphatidylcholine, is accelerated, producing a pattern of metabolic changes that mimics the changes observed in brains of AD patients, including the very high concentrations of GPC and low concentrations of acetylcholine. The cells apparently use a much larger proportion of their ATP for maintenance of membrane integrity, at the expense of other key functions ... meaning that not as much is available for the synthesis of acetylcholine, or for storage and use as a neurotransmitter.
So if the hypotheses of these recent papers are correct, Axona and MCT oil may help reverse some of the damage that is done in the Alzhiemer's brain when mitochondria dysfunction is triggered, including stabilizing the cell membrane composition and perhaps even increasing the availability of acetylcholine.
Dr Henderson (founder of Accera and inventor of Axona) has written a number of papers on the hypotheses behind Axona. I read them, but with glazing eyes and scrambling brain. He is clearly brilliant, I got that part, but sure didn't retain the details. And boy, did he have details!!! (Ask Marsh and Guy.)
Curious to see whether he actually discussed some of this, and now having some grasp of a little of it, I went back to look at his papers.
2004: "While increasing fatty acid metabolism may help prevent the disease, by the time clinical dementia is diagnosed (Stage II) irreparable damage may have occurred and reversal will be difficult. One strategy that might be effective is direct elevation of acetyl-CoA levels using ketone bodies (KB). Increasing acetyl-CoA levels will provide a substrate for acetylcholine and cholesterol synthesis and can be used in the TCA cycle."
2008: "Ketone bodies can bypass defects in glucose metabolism, and enter the tricarboxylic acid cycle in the mitochondria of neurons, where they are rapidly converted to ATP and precursors of acetylcholine. ...Ketone bodies increase acetyl-CoA levels in the mitochondria."
All of this stuff ties into insulin sensitivity, too, but my head hurts too much to try to sort through that right now. I need to take Dr Henderson in VERY small doses. <grin>
We are on day 3 of the Accera. Since I have been giving him 1T. MCT oil a day, I don't know if we will see any difference. The first 2 days I put the Accera and miralax into a cup of cranberry juice and used one of the 1 cup screw on top, storage containers that are so nice. Then I shake vigorouslly. This morning I used some iced coffee with cream and sugar. I think the coffee works best. Chocolate milk would work good too, I think.
Thanks for asking briegull. He is much better (AD wise) since we got him back home. Seems that he hasn't gone downhill, just back to where he was before all this happened. He doesn't feel all that well and is a little depressed. I'm thinking his body is probably adjusting to the new medicines and I'm sure that a heart attack takes a lot out of you.
I thought I would give you some encouraging news. My dh is stage 4 - diagnosed last July. I have been giving him 1/3 c. (5 1/3 T) of MCT Fuel once a day steadily for about 2 months. He is improving! He is more alert - is actually more "himself". He was able to preach a week ago and step away from his manuscript to tell personal stories. Before he has always had to write even the well known stories out and read them. I spoke to his dr about axona, but he had not heared of it and suggested I just keep doing what I am doing and that it is probably cheaper. I am to check to see if any pharmacies here have axona yet. Is there a reason to move to axona rather than keep on the MCT Fuel?
Just for the record, I tried giving him 1/2 dose in the morning and 1/2 in the afternoon. It did not work nearly as well. Also we tested this when we went on a short (3 day) trip and I forgot the MCT Fuel. He did alot worse - it was immediately very obvious.
He still has bad days, but they are not nearly as bad. I hope this is encouraging to someone else. Thank you Sunshyne for all your research and info.
Thank you Martha P for that encouraging news. I understand that Axona is supposed to be given just once a day. I don't have the MCT Fuel but have been giving MCT oil just once a day in DH's oatmeal. Your DH may have been worse on a trip even if he had taken the MCT Fuel. My DH is much worse if we're out of town for a few days and oh my....in the hospital....I hope he doesn't ever have to go there again!
Shannon, I checked with our prescription insurance, CVS Caremark, and a 90 day supply of Axona is $228.42. Our insurance will cover all but $38.07 for a 3 month supply. It's not covered by all insurance companies. You'll have to check.
I ordered my MCT oil. Joan has a link for it on her home page. The home page has changed but I think it's still there. Sunshyne says the MCT Fuel is better. Look for that before you order.
GuitarGuy, I called the mail order place and asked to speak to a representative. I think they handle lots of different plans. They put me on hold while they checked to see which plan we were on. You might want to talk to them personally.
Martha, thanks for the info. I'd been giving my husband 3 T of Fuel in the morning (recently increased from 2.5 T), and then 1.5 T of oil with lunch and dinner. I shall start upping his morning dose and see if that helps even more.
(I like the Fuel because it is an emulsified product, the closest thing you can get to Axona without actually getting Axona. But there's only so much orange juice I can get my husband to drink...)
My husband takes the OJ at breakfast. I put the MCT Fuel in about 1/2 cup of juice. I haven't tasted it, but he doesn't seem to mind it. I do keep reminding him how much he has improved and that helps the motivation!
I get the MCT Fuel over the internet at Vitacost. It is $7.77 a bottle and the shipping is $4.99 no matter how large the order. I use CVS Caremark also, but my ins said it was only possibly covered with a special request from the dr (who had never heard of it).
Is there a reason to use the Axona instead of the MCT Fuel?
(a) Axona is what has been tested in clinical trials. MCT Fuel has not.
(b) Axona is all caprylic acid (plus the additives for emulsification, which is good, and for minimizing gastrointestinal problems, also good, and possibly a few things that may help the body process the caprylic acid a bit better). MCT Fuel is 2/3 caprylic acid and 1/3 capric acid. Mostly, one might expect the capric acid to be metabolized the same way as caprylic acid but ... who knows.
So I think that Axona is probably a bit better -- certainly, we know more about it.
Plus I'll bet it tastes better. My husband doesn't complain about the orange juice either, but I tasted the supposedly orange-flavored Fuel. Eewww.
Marilyn, no, I haven't posted on fish oil, other than some stuff I tripped across while looking into saturated fats, and some stuff on safety (see below). Between what I'd already heard (which was enough to put myself and my husband on fish oil, with our doctors' knowledge and approval, and adding a lot more tuna and salmon to our diet), and what I saw when doing the saturated fat research, I think (if you couldn't already tell) that fish oil is a good thing.
The omega-3 in the fish oil may also increase the risk of bleeding when taken in large doses. One of the reported side effects of fish oil is a reduction of blood pressure, so be careful about giving it to people with low blood pressure or those taking blood-pressure reducing medicines. The impact on blood pressure appears to be dose dependent.
Also, look carefully at the contents of any vitamins/supplements. For example, vitamin E plays a part in metabolizing omega acids, so large doses of fish oil place high demands on the body’s vitamin E supply. To avoid this fish oil side effect, vitamin E is added to many commercial fish oil products. As a result, regular use of vitamin E-enriched products may lead to elevated levels of this fat-soluble vitamin.
I was giving fish oil and flax oil before DH's heart attack. When his medicines and supplements were reviewed before he left the hospital, the doctor said to keep him on both the fish oil and flax oil. The only Vitamin E he gets is in his Centrum Silver and the food he eats that contains it. I need to ask at our next appointment if he also needs to take Vitamin E.
On another note, Sunshyne, remember when we were giving coconut oil....before Sandy D sent you off on a brain bogging search to prove she was wrong? I had given DH one jar (1 Tablespoon a day) and almost all of another jar. From what you discovered in your research.....this maybe could have caused his heart attack! Big guilt bearing down on me.
Coconut Oil Bad For You? Hardly There is widespread misconception that coconut oil is bad for you because it is said to raise blood cholesterol and cause heart disease. The only "proof" is one four-decades old study. The study used hydrogenated coconut oil.
It is now known that the process of hydrogenation creates "trans fatty acids" (TFAs), which are toxic entities that enter cell membranes, block utilization of essential fatty acids (EFAs) and impede cell functionality. TFAs also cause a rise in blood cholesterol. These substances are not present in natural coconut oil.
In other words, a study based on hydrogenated coconut oil has no relevance to the non-hydrogenated coconut milk or coconut oil that you eat.
Widespread studies of coconut-consuming populations such as those found in Polynesia and Sri Lanka, show that "dietary coconut oil does not lead to high serum cholesterol nor to high coronary heart disease mortality or morbidity."(See endnote 1.) Other studies show no change in serum cholesterol level from coconut oil. (See endnote 2.) And if it is true that the herpes virus and cytomegalovirus have a causative role in the initial formation of atherosclerotic plaques (See endnote 3.), coconut oil may be beneficial in preventing heart disease. (See Benefits below.)
For further reading: Mary G. Enig, Coconut: In Support of Good Health in the 21st Century
bluedaze, from what I found while looking into coconut oil, Mary Enig is a paid consultant to, and spokesperson for, the coconut oil industry. She is rather infamous for her hypotheses, which go against everything the medical community espouses. She doesn't publish in any reputable journals, and she hasn't done any research for many, many years. She says the whole issue is a conspiracy by the rest of the edible oil industry to keep people from buying coconut oil.
Puh-lease. Conspiracy? Which the FDA and the American Heart Association are in on?
Trans fatty acids are bad, yes indeed, and you'd be wise to avoid them like the plague, but they have nothing to do with the subject of coconut oil.
It was when I was quoting this garbage without looking into such claims for myself that Sandy D suggested maybe the FDA and the American Heart Association would disagree about the health benefits of coconut oil. And I found dozens upon dozens upon dozens of studies, done in humans with coconut oil, ALL of which show that coconut oil is very unhealthy. The Polynesia studies showed that people in two communities who regularly consumed coconut oil have sky-high cholesterol levels. They did not have high death rates from cardiovascular disease, but this was apparently due to the rest of their diet, which in addition to being very high in fat was also very low in carbohydrates -- that is, a ketogenic diet. And the Sri Lanka "study" compared the amounts of coconut products Sri Lankans were eating, and decided that since they ate 130 coconuts per person per month 30 years ago and now eat a mere 100 coconuts per person per month, and the incidence of cardiovascular has risen, coconuts are obviously good. (Say what?)
Short-term gorging on saturated fats won't kill you, and I don't think Dazed did any harm at all to her husband. Long-term consumption of coconut oil is most definitely not going to improve your health. IMHO.
Sunshyne-isn't it a shame Sandy D is no longer posting. I think she needed us as much as we needed her. About the coconut oil-remember I said from the first that it is a saturated oil. There still is a great use for it-rubbing on your skin after showering :-)
I miss her, too, bluedaze, and I think she needs us. She is obviously not getting any support from her daughter, such a dreadfully sad situation. But she may still be reading here -- she did break her silence once, when Iowawife's husband died -- and hopefully we can help that way.
(I know, I know, you get to say "I told you so". Just don't mention Enig in front of me, ok? Raises my blood pressure.) (In case you couldn't tell...)
Thank you Sunshyne and Bluedaze for making me feel better. I think the reason I was feeling so guilty is that I was giving him the coconut oil without consulting his doctor and I never do that. I'm still giving MCT oil without consulting his doctor. I'm just so desperate to have something to make him better.
I also miss Sandy D. Sandy, if you're reading, please come back to help us.
Just a quick report on DH. He is having MCT Fuel 3 times a day. Much improved in my opinion, but when our son was here yesterday he pulled me aside and asked what meds his dad was on.....he could see improvement. That REALLY made me feel good! I had been afraid I was seeing improvement because I wanted to so badly.
Sunshyne, The reason I asked about fish oil was that I, too, am giving it to my husband and and we both eat a lot of salmon. His doctor says that is the only "nutraceutical" that he's really recommending--he offered to research Axona for me. What I wonder--and you are the scientist, not I-is that how much oil is actually good for a person to ingest? Fish oil plus Axona or MCT fuel--might it be overkill?
Very different types of oil, Marilyn, with very different health benefits. You'd want to give your husband both. Also, remember that MCT oil constituents are not metabolized or stored as fats -- they are metabolized as if they were carbohydrates, and used for energy right away. The only issue I see is controlling the total calorie intake so your husband doesn't gain too much weight. Mine is up about five pounds, but I'd been worried that he was losing, so I'm happy about that.
Sunshyne--My main concern about adding MCT fuel or Axona is that it will affect his bowel movements. Aricept was a nightmare when he first started and even 4 yrs later he has loose stools. This may be normal for him, but frankly, before dx I was not aware if that was the norm, and there's no way to find out now! Regarding weight, strangely his has increased, probably due to stopping regular exercise. His doctor says most AD patient lose weight, but then you know how it goes..... He is doing so well now regarding his mood--playful and joking again--I don't want to do anything that will put him back to a grouchy, touchy mode that lasted several years after dx.
Marilyn, you'd want to start slowly ... I was probably way overboard on being cautious, started with a teaspoon of the coconut oil a day for a week and gradually built up from there. (This was before I did all that research.) MCT oil is one of those things that people typically get used to, but of course divvi ran into a problem, I gather when switching from coconut oil to MCT oil. I suspect the emulsified product would be better for your husband if you want to give it a try.
Aricept can be purely awful because of the way in which it works -- my mother was like your husband. So when my husband's first neuro told me she didn't like Aricept and didn't want to prescribe it for us, I wasn't about to argue! His new neuro wanted something stronger than the very low dose of huperzine A that he's been on, so I (with fear and trembling) agreed to galantamine. He's been on it for almost a month now, and shows no signs of a problem, knock on wood, and does seem to be doing even better with that added on top of his MCT Fuel and Namenda.
My chiropractor and Naturopath both recommend at least 4 grams of fish oil (that is about 4 of the 1200mg capsules). That is a lot, but it is protective of the brain.
I received our MCT oil today. We took it by the spoon and there is not taste. It leaves your mouth oily feeling which is taken care of by eating something. If MCT fuel with the orange flavor taste bad, we will stick with the oil.
Charlotte, I think Fuel tastes mildly disgusting, even mixed with orange juice -- not awful, just not anything I'd be happy to drink every day. Definitely medicine. But my husband loves it in orange juice. There's a lady on the AlzAssoc forum who feels as I do, but her ADLO loves his orange juice, too. Maybe the effect that the AD has on their senses of taste and smell are actually helpful, this time ... ?