New to the Club! Anyone with any insight?

Submitted by MunchMan on Wed, 2010-06-16 15:33

Hello Everyone,


Ohhh where do I begin???


First, I’m a 31 year old male and cautiously optimistic about this protocol and appreciate what Sarah, Katman, and others have contributed to this site and I especially appreciate the work of Dr. Wheldon, Dr. Stratton, PaulJ, and whoever else explores this pathogen as a root cause for MS. I know this is a little longer than most blogs, but I hope to show that you are not alone, even though your MD’s, nurses, and sometimes your family members think you are bonkers. I also hope to gain some insight from people that have gone through the same experiences or people who have helped in any way to fight this disease.


I have had strange correlations with what I believe is this disease for 15-20 years. Starting from the beginning to now my symptoms have progressed as follows - recurrent upper respiratory infections (every spring and every fall) since I was 12, hives, arthritis, psoriasis, chills, swollen glands, kidney stone, occipital headaches, fatigue, optic neuritis, optic neuritis with fatigue, and then a possible Herx (which has lasted for at least 2 months now) from an T2 weighted MRI with gadolinium, or this could be heavy metal poisoning (currently being tested along with all my other blood work). But I had a strong urge for LARGE chocolate milkshakes during this for about 2 weeks which I have never done (I think this craving was a result in the increase of yeast during the “Herx”). And I am recently diagnosed with MS within the last 2 weeks with spots on the brain, and O-bands with myelin protein in the CFS. Bummer….


The most curious thing about all my symptoms seems to have progressed and ramped up in accordance to medication taken in the last 2 years to treat Sinusitis. I treated my normal sinusitis to avoid the dreaded upper respiratory infection with left over Biaxin in February. It went away fairly quickly. Hmmm…that was odd.  I then had surgery a month later to help with infertility. It took me 4 weeks to recover because of the dizziness, fatigue, and flu like symptoms (I didn’t know anything at the time of what was going on. Honestly, after speaking with the nurse I was taken my pain killer wrong, J, so I thought that was it.) 6 months later, optic neuritis. 6 more months later I had ON with fatigue. Did the MRI and all the symptoms came at once after I was done; dizziness, brain fog, swollen lymph nodes, chills, joint pain, fatigue, achy pains, diarrhea, bone pain, gluten and dairy sensitivy (which clears the brain fog.) This is why I believe it was a Herx. Seriously, I felt as if some dropped me off at the “You’re Screwed” train station with a one way ticket.


BTW, over the last 3-4 years I have consumed enough Red Bull, Monster, Rockstar energy drinks to keep a normal person awake for 20 years straight. I’m not speaking of one a day. I’m talking about one large in the morning, one large in the afternoon, and add another when needed. I know overconsumption is bad so I tapered off until I need to study for test. As I increased consumption to study this last fall; poof, I get Optic Neuritis and it would worsen with the drinks. Dr. said they were ocular migraines and said to stop the energy drink madness. I stopped until I had more test and a new baby in February – March. Poof!! Optic Neuritis again. Same thing. This time I went to get an MRI. What a funny little correlation, since caffeine helps the cystic state of CPn transform into a reticular state.


Just like all of you have done or will do, I have studied relentlessly for the last 2 months on the internet about MS, Lyme and all its brothers and sisters, and have found CPn in the last 2 weeks. I noticed one curious aspect of all these diseases and there ability to “mask” their symptoms as something else. All the symptoms look alike! When I told my Neuro’s nurse that I’m looking into Lyme and needed more time for the MS diagnosis, she said, “Well, they have the same symptoms. Why would you think you have Lyme?” “Okaaay, I have been bitten by two ticks in my life, there could be a chance. Duh!!” But there was something different with Lyme than with MS and my LLMD knows this: O-bands and myelin protein in the CSF; MS has them, Lyme normally doesn’t. I have read many forums, searched far and wide, to see something that might show a Lyme person with O-bands and proteins in the CSF. I finally found one person with these and has been treated with antibiotics and has been cured for many years now, also her whole family has “Lyme.” It’s a possibility that it was Lyme, but I think her disease leans more towards our newly found pathogen friend, CPn, especially with the coincidence of O-bands and myelin protein.


You see, CPn is the missing piece for me. Once I read all about CPn, it all made sense. My mother was schizophrenic (under investigation with CPn), with other complications that doctors could not make sense of throughout her body. She passed away with unknown causes. My brother suffered from hand tremors and other issues including depression. Once again, his death, too, is a mystery but probably driven by CPn. My father suffered from asthma, he administered shots when I was younger, but is better now and fights controllable Type 2 diabetes (probably not a relation). He also was a construction worker working most of his hours outside in the sun (possible mitigation of the disease). My older sister, I don’t know of anything that troubles her but she also didn’t live with us growing up until I was 10. My mother also had a hysterectomy when I was 7; things for her progressed worse since then. Mother, father, brother, and myself possibly infected before my sister moved in. I am hypothesizing that families with an MS relative also have parents, siblings, and anyone else that lives with them to have some sort of issue; which relates to a CPn deviation. The case in point is Sarah and Dr. Wheldon and many other families that get stricken with all of these fundamental symptoms from CPn, MS, and Lyme. We are talking about an infectious bacterium that can spread from person to person through the respiratory tract.


I have convinced my Neuro to refer me to Vanderbilt for possible antibiotic treatment. I have started the suggested supplements and added Creatine Monohydrate, a probiotic, and grapefruit seed extract for the yeast. Even though creatine labels itself as a sports nutrition supplement, it has so far been useful in decreasing fatigue in my legs and other muscles. Creatine helps your body replenish ATP, the main energy source of reticulate CPn. I don’t know of any ramifications posed, but I do know I feel better with this. Matter of fact, I’m ready for some right now. Yummmmm…….


I haven’t started taking NAC; I still don’t feel right and I know my body is depleted after these last 2 months and provoking a Herx right now would just plain suck. I plan on taking NAC in the next few weeks once I have supplemented for 1-2 weeks. I don’t know when I go to Vanderbilt but hopefully I will start before the trip. I hope, hopefully someone here at will inform, that they do this for early cases of MS/CPn. I have heard that Dr. Sriram likes to use antibiotic therapy as a last ditch effort. Why not treat the root at first? If you can pull some fluid from my body and use a polymer chain reaction to identify your pathogen, why not treat it?


I like my LLMD’s approach. ”Let’s give you some antibiotics to see if we can provoke a Herx!” Of course, he thinks its still Lyme.


This is the part of doubt that any of this could be possible so….


Am I inline with my assumptions?

Has anyone else had similar experiences?

What is the norm for Vanderbilt treatment on MS/CPn?

Would I be better off doing the protocol myself?

Would creatine fuel the reticulate CPn into a stronger enemy, producing more EB’s or produce otherwise detrimental activites?

Expressed concerns 2 paragraphs up.


I hope you enjoyed reading this, now that it’s off my chest, and I hope to have abbreviated stories/info in the future as time and health permits.


Thanks for listening,



Hi Munchman and welcome

I have RRMS and have been doing the Wheldon protocol for nearly a year - I undoubgedly feel better than before I started.  You sound well informed and a good candidate for the abx treatment.  If you can get to see the docs at Vanderbilt that's great - go for it - much better to have a doctor overseeing things if possible.

Good luck with it all and keep us posted as to how things develop.

with all good wishes



RRMs diagnosed 2008 (symptoms for 20 years). Also sinusitis, recurrent UTIs, IBS  Wheldon protocol began 31/7/09 Doxy 200mg, Azithro 250 3X week.  Supplements B12, D3 Vit C, multivit, Fish oil, probiotics, NAC, vit E, turmeric

Hi Agatha,I have seen you around and recall how you said you have had some success and do feel better in your postings. That's great!! It seems you and I are very similar with the progression and other symptoms. Do you take any "MS" drugs or is it all abx? I have seen some people with MS drugs and abx. I guess once a person is accustomed to their daily MS drugs, they depend on it and are scared of trying something that is going to hurt.  I have nothing to lose since this is all so new to me. Thanks for your comment, I hope to be one of the ones with positive progression and help others with this darn thing through abx's. Thanks again, Munchman

Started CAP on 06/29/2010 for RRMS. Dx w/ Brevundimonas Vesicularis in Jan '11 hiding in #20 tooth with root canal. Extracted 04/04/2011. Clinically dx with Bartonella at the same time. Recently found MPn.

Abx: 100 mg Doxy bid<

Well, no MS drugs here (I refused them), and a truly horrid diet of all things bad for you(I changed nothing in my life, except to add the abx protocol and stop using aspartame). I'd call myself 95-98% recovered. Welcome aboard the rollercoaster, Munch.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Hi Munchman, welcome.  Your family has really been through the wringer.  I hope you recover fully.  By the way, I'm flattered to be mentioned in the same breath with Drs. Wheldon and Stratton.  Perhaps some day I'll deserve it.

Your case sounds very similar to mine in some respects. Your energy drink story is familiar.  I was a scientist and then a technology entepreneur in the 1990s and took to drinking large amounts of Coca-Cola to get me through 70 hour work weeks.  This played a big role in promoting both bacterial and fungal infections.  It's really important to keep blood sugar levels under control - so avoid all fructose and minimize big slugs of glucose.  Really, drinks should have no calories at all.

As far as what steps to begin with, I think given the severity of your brain/CNS symptoms it's appropriate to begin with antibiotics and vitamin D, since the bacteria are the prime culprit there.  But I would get diet and nutrition right as quickly as possible.  As I've said before here, I think with a bad diet antibiotics are ineffective and, while they may slow disease progression, they increase die-off toxicities, and the ultimate result may be no improvement over non-treatment.  But on a good diet and with good nutrition to optimize the immune response and minimize bacterial reprodution, antibiotics can be extremely effective.

A complication when you have both bacterial and fungal infections is that too-rapid killing of bacteria leads to apoptosis of white blood cells and lets the fungal infection run wild.  When I first started a low-carb diet, I got a severe fungal infection and fungal meningitis that was very scary.  I think it pays to go at a steady pace where you get die-off symptoms but they're not excessively severe.

I would also immediately start taking substantial amounts of coconut oil.  Most neuronal damage is a stress response to starvation, because bacteria are stealing their glucose/pyruvate.  Short-chain fats are metabolized to ketones which provide an alternative fuel for neurons that the bacteria can't steal.  I think if you start taking a thousand calories a day of coconut oil, disease progression would be significantly slowed.  This buys you time to kill off the bacteria.

Another thing I would be sure to take is vitamin C. I developed scurvy at one point. Both fungi and bacteria increase vitamin C utilization and so infections can induce scurvy.  Vitamin C deficiencies can be very dangerous.

I have many more diet/nutrition tips but these are the most important points. Thyroid/iodine/selenium is next most important.

Good luck and I hope to keep hearing about your progress.  Congrats on your baby!


Blogger at 17-year chronic illness cured with diet and antibiotics, nearly fully recovered.

As regards:
Short-chain fats are metabolized to ketones which provide an alternative fuel for neurons that the bacteria can't steal.
Uh, medium-chain fats and long-chain fats can also be metabolized to ketones. And whatever the fatty acid chain length, that metabolism ("ketosis") only happens when the body is quite short of glucose. Even a thousand calories a day of coconut oil (or other oils/fats) won't necessarily put the body into ketosis, since most of the body can burn fats quite well even without ketosis. It's only the brain that can't burn fats, and thus demands either glucose or ketones (made in the liver) for fuel. So it takes a very severe restriction of carbohydrates, as in the full-bore Atkins diet, to put the body into ketosis.

Also, lots of bacteria can use fats for fuel. Cpn in particular isn't one of them, but it can still steal the ATP that the body produces from fats (or from ketones).

That said, as regards the moral of the story, it does indeed seem like a good idea to not pig out on sugars or other high-glycemic-index carbohydrates.

I am really glad you are going to the Vanderbilt doctors. I hope you make good progress to good health.

minocycline, azithromycine, metronidazole 2007-2009, chelation for lead poisoning, muscle pain, insomnia, interstitial cystitis (almost well), sinus, dry eyes, stiff neck, veins, hypothyroid, TMJ, hip joints (no longer hurt)


You do sound like you are on the right path. It boogles my mind why LLMD'S don't consider cpn a major pathogen. I also think you are correct in that most of us have been brewing this since childhood. Diabetes is connected. There is a bunch more articles but here is one. You are also right about schizophrenia being linked. Here is an article if anyone is interested. My father had emphysema. My mother had sever heart disease. Good Luck to you

200mg doxy daily, 500 zithromax mwf,flagyl 1000 m-fri.rifampin 2x daily,chloestryramine 2x daily

Hello Munch, if your doctor is willing to refer you to Vanderbilt, go for it and ask to see Prof. Sriram, since not everyone there is into abx.  It is far better to be treated by a doctor than doing it yourself, though.  It also helps to have a family member willing to ram the abx into you on the days you think that nothing is helping.       Incidentally, I had MS in a mild form for at least ten years before I met David.  His symptoms had also been developing slowly for a long time.  We both got a secondary Cpn infection at the same time and this led us rapidly to where we were when we started treatment.............Sarah       Avenues of Sight
Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Thank you Sarah.


I believe you have been an inspiration for many of us including myself. Since this whirlwind started, I'm seeing the trials and tribulations that people go through when they are sick and appreciate everyone and anyone's moments to help someone else. Caring can be infectious to anyone that accepts it and passes it on. Dr. Wheldon and yourself have consistently and openly been advocates of abx treatment when fighting these diseases, therefore all I can tell you both is "Thank you." I strongly believe that if I do not show positive progression on abx, I know we are closer than ever to finding other causes and will be able to fight the culprit in the short future because of the work the abx community has done. It's hard to believe our creator made us imperfect and allow us to consume ourselves for no apparent reason or being "fooled" to do it. Anyways, before I get to much on my soapbox, Thank you Sarah and Dr. Wheldon.


Started CAP on 06/29/2010 for RRMS. Dx w/ Brevundimonas Vesicularis in Jan '11 hiding in #20 tooth with root canal. Extracted 04/04/2011. Clinically dx with Bartonella at the same time. Recently found MPn.

Abx: 100 mg Doxy bid<

Thank you everyone!

I still haven't heard anything from my neuro about TN; hopefully I will here something soon. If not, there is always Canadian meds. =)  

Paul – Thank you for your insight, I like the scientific side that you bring, and I agree totally with the diet; since I developed extreme gluten and dairy sensitivity with the onset of symptoms, I now don't eat out as much and soon to eliminate it all the way but if I do I keep it sensible. I'm adding the coconut oil as well.

Lee - I'm sorry about your family. Has anyone else thought that a "bad-health" curse has been following your family? Seriously, as if someone has a voodoo doll and assiduously gouging at everyone in your family? I believe the puppet master has been found. BTW, great links, too.

Janice – thanks for the support! Are you under MD care or a maverick? 

Mac- I agree, I don’t like the idea of shutting down my immune system especially if that is not the cause of all of this.Thanks again everyone. It’s nice to see support from other people that are going through this unfortunate mess and I hope to support others including ya’ll along the way. Image removed.


I am also working on a excel spreadsheet for daily symptoms that I would love to share as soon as it is completed. This will help show symptoms during the long term treatment which come and go and eventually get better. I know 2 weeks ago I felt arthritic pain, muscle pain, etc, that I am no longer feeling. Now I have the twitches and other continued symptoms! It will help the MDs to see progression of the treatment as well.


Talk to ya'll later and everyone has a great day as much as possible!




"The person who gets the farthest is generally the one who is willing to do and dare. The sure-thing boat never gets far from shore."
-Dale Carnegie


Started CAP on 06/29/2010 for RRMS. Dx w/ Brevundimonas Vesicularis in Jan '11 hiding in #20 tooth with root canal. Extracted 04/04/2011. Clinically dx with Bartonella at the same time. Recently found MPn.

Abx: 100 mg Doxy bid<

Mackintosh - I'd be curious to hear what "all things bad for you" means.  Conventional dietary recommendations are mostly wrong, so defying those recommendations generally improves health.  Oddly, this has been shown in the Nurses Health Study - the smokers / non-exercisers who ignore health recommendations fared better in many ways than the nurses who obeyed all the health advice!
Blogger at 17-year chronic illness cured with diet and antibiotics, nearly fully recovered.

Hey Munchman         

Welcome to the club.  You sound a bit like me with all the nergy drinks.  While I wasn't on them as often as you, I did my fair share for a while in the first year or two after I started the CAP.

A related thing I did and stopped was I used to take caffeine pills all day long.  200mg of caffeine about 7 or 8 times a day.  I know the energy drinks have their fair share of caffeine so I'm guessing that's part of why you used them.

Anyway, as I said, I'm not on caffeine anymore, ever.  Of course, there may be something that's got a small amount of caffine in it but it's miniscule at best, such as the decaf version of 5 hour energy which has 6 mg of caffeine each.  When you contrast that to a cup of coffee, which has around 25 mg, you can see how miniscule we're talking.

I hope you'll post if you have any questions.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

Thanks for the advise John.


I have cut out most of the caffiene mostly out of fear of "it" coming back on. I now enjoy maybe 2 cups of black coffee in the morning once I get to work. This will soon end. The soft/energy drinks I have cut out; I've really lost the taste for them. I do have a question for you. I noticed your RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999. It looks as though you progressed pretty excessively. Are you now better than before?


Thanks, MunchMan

Started CAP on 06/29/2010 for RRMS. Dx w/ Brevundimonas Vesicularis in Jan '11 hiding in #20 tooth with root canal. Extracted 04/04/2011. Clinically dx with Bartonella at the same time. Recently found MPn.

Abx: 100 mg Doxy bid<


I really wish I was better but I'm not.  I've gotten progressively worse as you pointed out.  I'm hanging on, just below EDSS of 7 which is basically bed ridden.  I still can get around my house in my walker but stairs are out of the question as is standing for more then about five minutes.

best, John

RRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
nac 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day


I'm sorry and I hope i didn't come across as brash. 

You know, I understand things get worse before they get better and this is a long term treatment. I saw that you are going to the MD to tomorrow. Are you getting your results back for your blood work? I do hope the best for you and soon there will be a turning point and just know there is huge support here for you.


Started CAP on 06/29/2010 for RRMS. Dx w/ Brevundimonas Vesicularis in Jan '11 hiding in #20 tooth with root canal. Extracted 04/04/2011. Clinically dx with Bartonella at the same time. Recently found MPn.

Abx: 100 mg Doxy bid<

I drink a cup of coffee every morning and while I wouldn't overdo it, I don't see any reason to cut coffee completely.  Coffee drinkers have lower rates of Alzheimer's which is probably caused by CPn, so that suggests a cup of coffee might be beneficial.  I find I do better on coffee than green tea, which I used to drink.  The tea has too much oxalate and promoted fungal growth.  No such problem with coffee.
Blogger at 17-year chronic illness cured with diet and antibiotics, nearly fully recovered.

Norman - I was using "short-chain fats" colloquially to include medium-chain fats.  Basically, all 12-carbon or shorter fatty acids are predominantly metabolized in the liver to ketones, since they have no structural use.  14-carbon and longer fatty acids have structural uses and are metabolized throughout the body, not just in the liver, and generally in their metabolism are either (a) burned all the way to water & carbon dioxide or (b) are partially burned and recycled into other lipids for local use.  They are not released into the circulation as ketones for uptake by neurons.

The liver will create ketones from proteins or long-chain fats when the body is short of glucose, but it will create them from short- and medium-chain fats whenever those are available, regardless of glucose status.

Bacteria can use fats for fuel only when they have oxygen available, which isn't the case normally in the body.  And as you say CPn and other chronic intracellular pathogens generally lack this ability entirely. 

To be clear:  I am not recommending an extreme low-carb ketogenic diet.  I am recommending creation of fairly abundant ketones, along with sufficient but not excessive glucose. 

It's quite right (with a few exceptions, e.g. red blood cells, some kidney cells) that only neurons cannot burn fats. The reason I focus on neurons/brain/nervous system is that's where the most intractable problems from chronic bacterial infections come.  Other cells can survive on fats even if bacteria steal all their glucose/pyruvate, but neurons cannot unless ketones are made available.  So the most severe symptoms from chronic bacterial infections are in the brain and nervous system.


Blogger at 17-year chronic illness cured with diet and antibiotics, nearly fully recovered.

Paul, where are you getting this stuff? Everything else that I can find says that ketogenesis only takes place when there is a lack of carbohydrates. I did find some references to medium-chain fatty acids being a bit more ketogenic than longer-chain fatty acids, but that still involved huge quantities of them and severely-limited supplies of carbohydrates. For instance, Wikipedia refers to medium-chain triglycerides being more effective at producing ketosis, but even that talks about diets having 60% or 45% of energy from medium-chain fatty acids -- which would be difficult or impossible to do with coconut oil, which only has about 50% medium-chain fatty acids to start with, even before you mix it with other things. Instead they use "MCT oil", which is described as being expensive, and which I take to be this sort of stuff. Another article talked about ketogenic diets using, in some cases, only 30% MCT oil, plus 30% other oils. That's more approachable using coconut oil, but if the rest of the diet includes normal quantities of carbohydrates, you may not get significant quantities of ketones at all, since that study limited carbohydrates to less than 15% of dietary energy, "reduced to a lowest value of 12% if necessary". In any case, if you're getting meaningful quantities of ketone synthesis, you'd likely be able to detect it via "acetone breath" or, more objectively, via diabetics' "Ketostix" (as Atkins recommends to people on his diet). Have you tried those tests? There are always trace quantities of everything (including ketones) floating around, chemistry being rather random on the molecular level; but quantities that can be used as serious fuel sources are another matter: for something to be a meaningful fuel, there has to be a lot of it in the blood.

In any case, it's lauric acid in particular that's in question, not other medium-chain triglycerides. I thought it'd be easy to look up the metabolic fate of lauric acid, but it's surprisingly difficult. This article says that unlike shorter fatty acids, lauric acid doesn't all go straight to the liver after digestion; instead, 70% of it gets processed like longer fatty acids are -- packaged into chylomicrons and sent through the lymphatic system into the bloodstream for use around the body. (The MCT oils advertised on the web seem, at a casual glance, to consist almost entirely of shorter fatty acids, so this further limits the relevance to coconut oil of dietary studies using "MCT oil".) Some of the lauric acid eventually gets stored in fat -- this study found that in Polynesian coconut-eaters, a bit more than 10% of their body fat consisted of lauric acid. The study estimated that 80% of their fat intake was from coconuts, which are about 50% lauric acid; so if all fatty acids were treated the same, lauric acid would be 40% of their body fat, not 10%. Instead, most of it seems to be grabbed by the liver and turned into other things -- but not necessarily into ketones; it might go through beta oxidation, then become available for all the things acetyl-coenzyme A is used for; or, as in this paper, it might get elongated into myristic acid.

As for the idea of focusing on the brain, the sort of modest high-fat diet you're recommending seems to me to be more useful outside the brain, where the energy source switches from glucose to fatty acids in response to the sort of relatively-mild dietary shifts you recommend, while the brain keeps running on glucose. (It's the blood-brain barrier in particular that stops fatty acids; neurons elsewhere can burn fats.) It'd take, according to my reading, a more extreme high-fat diet to influence brain metabolism much. And even then, you wouldn't necessarily improve the fate of infected neurons, since instead of having glucose stolen from them, they'd have ATP stolen, which might be worse for them. It's ATP theft that Stratton blames for porphyria.

Oh, and I didn't say "and other chronic intracellular pathogens"; I talked only about Cpn in particular. I'm not disagreeing -- I don't know enough to either agree or disagree about such a general proposition -- but please don't put words in my mouth. At least one important chronic intracellular pathogen, tuberculosis, can burn fats just fine. (Yes, it needs oxygen to do so, but the body is generally supplied with oxygen; that's what the lungs and red blood cells are for.)

Norman, I must admit I don't comprehend some of what you're talking about, but I am hugely grateful you continue to supply links and references so that folks like me can research the SOURCE of your comments.

Generalized assertions, no matter how authoritative the phrasing, must be considered suspect without attribution. 

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

By the way, in case it's not clear, the question I started with was a serious question, and the answer that "it's a vague guess based on various things I read" is not one that I'd laugh at. It's a pleasure having someone here who comes out with interesting hypotheses, even if I partly disagree with them -- a welcome change from stuff like Rife machines, where there is so little probability that the idea is correct that it's not even an interesting exercise to debunk it.

Norman - Like MacKintosh I also appreciate the effort you put into your posts, including links and citations.  It's a pleasure to delve into the science, and I'm happy to be corrected when I say anything in error. The statement that “12-carbon and shorter fatty acids are predominantly metabolized in the liver to ketones” is one I've seen repeatedly in biochemistry texts and on several scientist blogs.  I will search for peer reviewed publications when I have time. For now I’ll only note that the papers you cite are consistent with that claim: In the rat hepatocyte paper, first of all this is tracing the destinations of the lauric acid carbons, not the ultimate destination of the fatty acid stem. (It’s the stem, not the Acetyl-CoA 2-carbon units, that are made into ketones.) So it’s not directly on point. Nevertheless, what’s notable is the small fraction of lauric acid carbons that ends up in longer fatty acids. This could occur either through lauric acid elongation or through partial beta-oxidation of lauric acid, stripping carbons, followed by lipogenesis. In Figure 1b about 20% of the carbons ends up in longer fatty acids, but in Fig 2a only about 1% has appeared in longer fatty acids. You’d expect at least this much on several day time scales from carbon recycling alone. In similar C14-labeled experiments with the 18-carbon PUFAs, the carbons are predominantly recycled into palmitate, cholesterol, and other lipids. (Here’s one paper to get you started: See Tables 5, 6 and text.) It seems that linoleate carbons are as likely as lauric acid carbons to become part of palmitic acid. This suggests to me there’s not a huge amount of lauric acid elongation going on. In the 1969 AJCN paper, Polynesian tissue fatty acid ratios, as you note adipose tissue lauric acid was a smaller fraction than dietary lauric acid. This indicates that some goes into chylomicrons (or into triglycerides packaged in the liver), but doesn’t suggest that’s the predominant disposal route. Two other points: (1) lauric acid was the only 12-carbon or shorter fatty acid that reached adipose tissue. About 20% of the fatty acid content of coconut oil is 10-carbon or shorter and goes entirely to the liver. (2) Levels of lauric acid in blood lipids were very low. This indicates that if lauric acid does go into chylomicrons or triglycerides, it doesn’t stay there long – not overnight. It’s possible that adipose cells may concentrate a small fraction of lauric acid that does reach the blood. In the 1992 AJCN paper, which you cited twice, the statement that only 25-30% of ingested lauric acid goes the portal vein route to the liver is immediately in tension with the next statement that 95% of ingested medium-chain triglycerides go to the liver via the portal vein. Note that “medium chain” triglycerides normally means that they are predominantly composed of 10-carbon and 12-carbon fatty acids. So MCTs often have lauric acid as one or several of their fatty acids. Coconut oil fats are predominantly in the form of triglycerides. I haven’t read the cited papers yet (refs 25-28) to sort this out. So – deserves further research. But, to clarify the issues, let me put some numbers to my argument. 1,000 calories of coconut oil will produce on the order of 100-150 calories ketones which equals about 25% of the 480 calories per day needed by neurons. (So, I don't care where 80-90% of the lauric acid carbons go - as long as 10% go to ketones and reach the nervous system.) Glucose transport into the brain will supply about 480 calories. If CPn or other bacteria are stealing 75% of neuronal pyruvate, leaving only 120 calories, then the coconut oil would double the available energy substrates for neurons. This would, I suggest, substantially reduce neuronal stress.
Blogger at 17-year chronic illness cured with diet and antibiotics, nearly fully recovered.

I don't understand the claim that
"It’s the stem, not the Acetyl-CoA 2-carbon units, that are made into ketones."
What do you mean by the "stem"? I thought the whole fatty acid molecule was one big stem, and in beta-oxidation all of it could get broken down into acetyl-CoA pieces, which then could get made into ketones (or re-assembled into longer fats, or burned for energy).

As for the rat hepatocyte paper, they weren't trying for a 100% accounting of the added carbon-14 radioactivity; for instance they started their analyses of the hepatocytes by throwing away the culture medium (which no doubt still contained some of the original lauric acid, plus some of whatever it got turned into). So it's wrong to read the paper and draw any conclusions from the absolute magnitudes of their numbers; only the relative magnitudes are meaningful.

As for the presence of acids shorter than lauric acid in coconut oil, yes, I see I was wrong there -- too hasty in looking it up.

As regards:

"Levels of lauric acid in blood lipids were very low. This indicates that if lauric acid does go into chylomicrons or triglycerides, it doesn’t stay there long – not overnight. It’s possible that adipose cells may concentrate a small fraction of lauric acid that does reach the blood."
Yes, generally lipids in the circulation don't stay there long: the bloodstream is a transport mechanism, not a storage space. Fasting blood draws, like the one they did, mostly measure fats released from adipose cells (or from the liver). But I'd guess it's the liver, rather than the adipose cells, being choosy: if you figure that (1) after a meal, the liver grabs 75% of the lauric acid before it gets to the adipose cells, and (2) when the adipose cells release it into the bloodstream during fasting, the liver grabs 75% of the remainder, then you have a tolerable approximation of their numbers.

As regards:

"In the 1992 AJCN paper, which you cited twice,
Did not!
the statement that only 25-30% of ingested lauric acid goes the portal vein route to the liver is immediately in tension with the next statement that 95% of ingested medium-chain triglycerides go to the liver via the portal vein. Note that “medium chain” triglycerides normally means that they are predominantly composed of 10-carbon and 12-carbon fatty acids. So MCTs often have lauric acid as one or several of their fatty acids."
That paper seems to me to be using "medium-chain" to not include lauric acid; so I don't think there's any real tension there, just an attempt to contrast lauric acid with fatty acids shorter than it (plus perhaps some mildly-sloppy wording).

As for your numbers, I doubt that even 10% ketone production is going to occur unless you restrict carbohydrate intake. (And when ketogenesis does occur, it's not only the brain that burns the resulting ketones; other parts of the body do too -- so it might not be just 10% going into ketones, but could be a lot more.) Also, when bacteria steal fuel, the body commonly responds by supplying more fuel to the affected area, to overcome the theft. Stealing ATP, which is at the end of a long synthesis chain, is going to be harder to overcome than stealing pyruvate, which is closer to the source. Actually, according to this paper, the main substance stolen, at least in Chlamydia trachomatis, seems to be glucose-6-phosphate, which is even closer to glucose -- just one step away. So theft of carbohydrates might be a complete non-problem, except of course that it allows the bacteria to grow and thrive.

As regards disappearing paragraphs, I don't know what might be going on, or whether they are still missing; but if they are, you might try adding them to a new post.

Hi Norman,

Ketones have oxygen and the COOH alpha-end of a fatty acid is readily made into a ketone but not the oxygenless 2-carbon units stripped off during beta oxidation.  Yes, the whole fatty acid including the stem can be oxidized, but in conditions of ATP and heat surplus that's not normally what happens - a fatty acid that is being burned for disposal reasons will be partially oxidized and then the remainder recycled.  It's not uncommon for the stem to be released as a ketone body.

Your numbers for the liver grabbing 75% of lauric acid are plausible.

According to physiology texts, the transport of glucose into the brain occurs through a concentration gradient, it depends on the difference in concentration between blood and brain.  So there is an upper limit to glucose transport under normal circumstances.  Then glial cells take the glucose, transform it into more energy-rich substrates farther down the glycolitic pathway, and pass substrates like pyruvate, lactate, and glucose-6-phosphate to neighboring neurons. If CPn is able to intercept these substrates, then the neurons can become energy-deprived even if the glucose reaching glial cells is normal.

I'm making a hypothesis that this CPn substrate-interception is important, but it fits with the cytopathology of neurons in MS, Alzheimer's, Parkinson's, and other brain diseases that may be CPn-caused.  The neurons have a characteristic pathology of hypoglycemic or hypoxic stress.  Moreover, on a gross level the mood and cognitive changes in MS and Alzheimer's closely resemble those found in hypoglycemia.  How does this occur with normal glucose levels in the brain?  The substrates must be getting intercepted downstream, within the neuron.

While mitochondria generally can burn ketones, they are preferentially taken up by neurons.  In the absence of starvation I bet they primarily end up in the nervous system.

I've previously posted the story of an Alzheimer's patient who substantially recovered cognitive function consuming 12 tablespoons coconut oil per day.  I don't see any explanation for this result except that on the order of 10% of the coconut oil calories are reaching neurons in the form of ketones.


Blogger at 17-year chronic illness cured with diet and antibiotics, nearly fully recovered.

Porphyria and coconut oil:

I have read-with great interest--a billion posts.  :)  Optic neuritis--no small feat.  I actually have been studying the Cpn connection for months.  Currently have been trying to resolve porphyria and the high carb issue.

Regarding ketones and coconut oil.

Is there any evidence--or anyone's opinion or thoughts-- will the coconut oil help to improve the porphyria?  Would like to reduce carbs. 

I have a small business and having trouble functioning--need to resolve porphyria.   

I started coconut oil two days ago.








There's a reason why it's called "beta-oxidation", which is that oxygen gets introduced: the fatty acid molecule gets partly oxidized, as it is being split into parts. The two-carbon pieces that get split off, rather than being "oxygenless", are part of acetyl-CoA molecules, where CoA is "coenzyme A" (which doesn't get burned for fuel, or converted into anything, but rather split off and reused), and "acetyl-" denotes a CH3-CO- group, a relative of acetic acid (CH3-COOH). The acetyl group is the part that gets used for fuel: either burned immediately, assembled into fatty acids, or made into ketones.

The reason I'm not citing sources for this sort of stuff is that I don't think there's any biochemistry text that'll tell you differently; choose whichever you prefer.

I know it's an old thread, but I've been reading on your site researching the chronic use of abx and could not resist from butting in...

Paul is right stating that MCT oil, of which coconut oil is a rich source, is metabolized by liver into ketones. Norman thinks that ketones are produced only during ketosis, when carbs are low, but this is not the case at all (just read the Wikipedia's references on MCT oil). And until I read the last post by Paul I too wanted to bring up the ample anecdotal accounts of people with Alzheimer's and Parkinson's improving with MCT oil supplementation, exactly because resulting ketones provide the alternate fuel for the brain.

My other interest is fasting and its therapeutic effect on various chronic diseases. So, I just wanted to remind that ketogenic diet was originally invented back in the 1920s (way before Atkins) to mimic the metabolism of a fast. In your place I would not discount fasting as a means of a cure. Just go into it cautiously, starting with one day a week, and you will be amazed.

Uh, I've already been through some of those references; and they only confirmed me in my idea that ketones are only produced in serious quantities during ketosis. If there is one which says something to the contrary, please point it out. (Biochemistry being the random thing it is, there are always small quantities of everything floating around; but serious quantities, usable-for-fuel quantities, are another matter.)

Personally, I've been messing around with fasting for a while, now. By itself, it doesn't seem to do much for me. In combination with metronidazole, as I've described, it has some pretty extreme results.

You are right that ketones are produced in serious quantities during ketosis. But the liver is a "dumb" organ and will produce ketones out of MCTs it encounters in blood. That's the principle behind the long proven practice of supplementing MCT oil both in ketogenic diets and for improvement of brain function in patients with neurodegenerative diseases on normal diets.

 You too can try it, you know, and see for yourself if it works for you. It's not that expensive. 

As for your experience with metronidasole while fasting, I saw it and left you a lengthy reply this morning. Unfortunately, I included a link to a protein cycling blog and it was flagged by the software here as a potential spam. I hope the moderators will post it eventually. I am very curious about your reply. 

Hello Munch Man

You said 

over the last 3-4 years I have consumed enough Red Bull, Monster, Rockstar energy drinks to keep a normal person awake for 20 years straight 

Ha ha ha that cracks me up ....Are you sure you weren't drinking it when you made your original post?

But seriously I think that stuff is poison so glad you're off it 

I didn't read everyone elses post but I did read Paul's I agree .....Build up you nutritional resovior then start the abx 

I have been using Caffeine/NAC Antibiotics combo  for a short time and have been getting good results 


DAILY:  NAC 2400MG , DHEA sublingual , vit D3 , multi vits,./ Three times  a week: B12 injections (Hydroxycobalamin). Deer antler./  Once every few months methyl B12 Methyl injections

Actually I can't really try it. Two years ago, I could have; but now I scarcely have any disease left to try it on. I suppose I could test the liver thing in particular: eat modest quantities of MCT oil or coconut oil, on top of a normal diet, and see whether I get acetone breath from it. But I'm not even sure if you're asserting that I would get that result.

No, you won't get acetone breath from consuming MCT or coconut oil. Ketones in breath and urine appear only in the period of adaptation to fast approaching ketosis, when there is abundance of ketones in plasma but the body is largely not ready to utilize them (because many cells need to "turn on" required genes, which takes time, because they have not used them in years). Those who fast frequently transition onto ketosis smoothly, without acetone breath. 

Ketones are utilized by brain cells in neurodegenerative diseases, because then the glucose uptake by neurones is impaired. Those neurones are hungry and so they mop up ketones quickly. That's why there is a clear improvement in brain function with MCT or coconut oil supplementation in Parkinson's or Alzheimer's (without acetone breath and without ketosis proper).

I see that my post on your flagyl fast thread was not posted. Too bad. I guess people here are not interested in free exchange of ideas...

Still, I'd like to point you into a right direction. Of course, I can't provide links, because that's considered spam here, so you'd have to google to find that info yourself. You need to read on "autophagy and infections" and "autophagy and autoimmune diseases" (<-- google) to learn the role autophagy plays in your disease. Hopefully in the process you will find out that nothing upregulates autophagy as well as fasting... But I do not wish to repeat my post again, especially since moderators did not find it usefull..

Good luck to you in your recovery!



I'm with you on ketones only appearing in the urine when there is an excess of them, and the body needs to dispose of them; but that's why I specified breath, rather than urine. If there's acetone circulating in the bloodstream, plenty of it will get breathed out, as it's rather volatile.

As for the idea that you're being oppressed, don't be silly; the moderators here are quite liberal in what they accept. They may simply not have gotten around to your post yet. In any case, it's easy enough to post links without triggering the spam filter: just post them as text, not as active hyperlinks. If the rich-text editor insists on activating the link, either switch to HTML input, or say something the editor doesn't recognize as a link: "foo dot com slash whatever" rather than "".

Norman, Thanks for responding to the assertion that FrequentFaster makes about feeling over-moderated. I'm sure, once s/he has spent more than two weeks as a member of this site, it will become very apparent how open and liberal this site actually is.

Per FF, "I see that my post on your flagyl fast thread was not posted. Too bad. I guess people here are not interested in free exchange of ideas..."

FF, you will know within SECONDS of hitting the 'enter' button whether your post is accepted, because it will or will not be posted. Too-numerous links, links to known malware sites or known spam-generating sites (and to some commercial sites) are trashed by the spam filter, not by site monitors.   Without the spam filter, every member here would be inundated with spam and malware 24/7.

If your post does not appear within a minute, try re-posting it without any links,  or by entering your site referrals in the manner Norman suggests. 

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Norman, acetone is one of ketones and ketones are fuel => body pees them out and breathes them out only when they are in excess. This happens only during adaptation, when things are still not working right. Similar thing happens with glucose, when it is in excess: kidneys remove it from plasma too.

But I'm getting tired of our one-sided exchange. Why argue about such a simple thing, when not just me but many people, starting with Paul and ending with Wikipedia, tell you the same thing, and yet you apparently think that we are... not quite on the level...?? It's so simple. You buy that MCT oil --it's only $20 or so-- and see for yourself that it does affect your mood and attention.


As for me feeling oppressed, why was not my post posted? I had only one link there, a reference for your convenience, to a protein cycling blog authored by a PhD in biochemistry, who explains autophagy in very friendly terms. That's why I offered it (otherwise, I mostly read scientific papers, which may be a heavy and boring read for people, especially when they are not well).  

And I can't repost it. I put a lot of time into it. It will be a long while before I will feel up to it again. 

Dude, the lungs are different from the kidneys. The kidneys are specifically designed to hold in substances we want (like fuels), and piss out the others. The lungs, on the other hand, are designed for gas exchange. They don't feature active transport of gases; gases just diffuse in and out, across thin membranes. If you've got acetone in your blood, some of it gets breathed out.

That's basic physiology. I don't particularly care how many people who are ignorant of basic physiology tell me I'm wrong. And while you've told me to go read the references in Wikipedia, you were silent when I asked, specifically, which reference contradicted anything I'd written. I'm not going to troll randomly through those references to look, and then come back and have you tell me that I must have looked in the wrong places. You also still haven't supplied the link you think is useful, even though I told you how to do it without exciting the spam filter. (No, I'm not going to troll through Google results either -- not for someone who doesn't show me the basic consideration of posting the damn link.)

It would also help if you realized that I have nothing in particular against your agenda. That fasting or a very-low-carbohydrate diet creates ketones -- certainly; that MCT oil helps push towards ketogenesis -- certainly; that this is useful medically -- maybe or maybe not, you haven't proved it, but it's certainly plausible. (Well, for epilepsy, it's standard medical practice; but we don't have many people who suffer from epilepsy here.) I just disagree on the idea that you can eat a moderate amount of MCT oil, on top of a normal diet, and get serious generation of ketones. That doesn't mean your agenda is wrong; it just means that people who try it have to try it seriously, and take major quantities of the stuff, or almost totally avoid carbs (or fast). The "twelve tablespoons a day" of coconut oil that PaulJ mentioned above falls into that major intervention category: at 15 ml/tablespoon, 0.925 g/ml, and 9 calories/g, that's 1500 calories/day of coconut oil.

I'm sorry your post got nailed by the spam filter, but we do need spam filters here; even the spam that gets past the spam filter is enough to be annoying. The way to deal with it, here and elsewhere, is to keep a copy of anything long you compose.

Ha! Dudette, perhaps? I see that you're absolutely set on remaining the rightest of them all.

First, I missed that bit about 12 spoons of coconut oil. That must be for a real ketogenic diet. I know that a beginner will get a diarrhea with anything above a tablespoon at a time. And yes, this amount of oil, if you manage to consume it while still on a regular diet, will give you enough ketones to be smelled on you breath. 

Second, I have no agenda, other than share my excitement and delight about my recent discovery with others. In any rate, you'd have to agree that a water fasting is a hard sell -- there is absolutely nothing one can sell to go with it!

Third, I have not seen such a trigger-happy spam filter as on this board and I've seen many.

Fourth, it's up to you to fix your problems rather than insist that your rare guests must jump hoops in order to accommodate you with reference links.

Fifth, your rich-text "feature" is a real pain.

And finally, I did not like your tone in the last post. I just would like to remind you, in case you forgot, that when you find yourself surrounded by idiots, like you are now --my sincere condolences to you!-- the rule of thumb is that you're probably at fault.

I get no points for educating you. Ta-ta!


That's the only agenda I meant. As I said, I have nothing against it, except when you trample over the facts in your haste to share your "excitement and delight".

Please realize that you're doing a pretty poor job of "surrounding" me. PaulJ was arguing with me at first, but you're the only one arguing at present. Wikipedia isn't arguing with me; the Wikipedia ketogenic diet page speaks of diets containing 60% or 45% of energy from MCT oil, and that with carbohydrates limited. So all I see arguing with me is one anonymous poster who repeatedly avoids providing references, instead relying on the-spam-filter-ate-my-homework excuses.

Agreed on the rich-text editor being annoying; that's why I write using the HTML input feature. (If you click on "Input format" below the text box, it gives you a choice.)

This website runs Drupal, which offers a variety of spam-blocking modules. There's a fair chance that there's a better one than the one that's installed at the moment. The Drupal folks themselves have complaints about overzealous spam filtering.

Sorry for imputing the wrong sex to you.

"Third, I have not seen such a trigger-happy spam filter as on this board and I've seen many."

I guess you'll just have to learn to adjust to it or forego posting here. The work-around is pretty simple.

" Fourth, it's up to you to fix your problems rather than insist that your rare guests must jump hoops in order to accommodate you with reference links."

From where I sit, I don't see that Norman is the one with problems to fix. You'll have to operate within the limitations of the website design here, which is not debilitating or overly difficult to do. 

"Fifth, your rich-text "feature" is a real pain. "

 Odd, that it's worked fairly well for so many here, for so many years.  If you're a web designer, you might offer your expertise to the site owner.

" And finally, I did not like your tone in the last post. I just would like to remind you, in case you forgot, that when you find yourself surrounded by idiots, like you are now --my sincere condolences to you!-- the rule of thumb is that you're probably at fault. "

Totally agree with the surrounded by idiots part.  I have often told my subordinates at work that, if they had a problem with one person, the fault could lie with either one.  But, if they have a problem with most people, then it's likely THEY are the cause of it.

But it isn't Norman who's got a problem, an agenda, an attitude and is rapidly alienating people.  Two weeks on a site is not enough time to thrust oneself into people's 'faces' critiquing, editorializing, or attacking.

If you don't want to debate issues, then don't post; it's very simple.  If you feel you're right, it's not enough to say "Because I said so".  You need to provide documentation and validation for your statements, or deal with the questions and comments they garner.  

And, if you don't like the make-up, construction of, filters, style, or colorways of this website, you are always, of course, free to create and establish one more to your own liking.  

Now, can we get back on topic, please?  I, and I'm sure several others, was actually learning something from the conversation.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Hi Norman, how is it going? Here is a paper you may find interesting: freepdfhosting dot com/277e896fa5.pdf Get it quickly, or it may disappear soon, being in possible violation of copyrights.

REVIEW Autophagy, inflammation and neurodegenerative disease


Here we review the significance of autophagy in neurodegenerative disease, highlighting its possible importance both in infectious neurodegenerative disorders (e.g. HIV-1-associated neurocognitive disorder) and in immune-mediated neurodegeneration [e.g. multiple sclerosis (MS)].

Thus, autophagy may be involved in a variety of non-infectious neurodegenerative diseases, and we speculate below that changes in neuronal autophagy also may contribute to MS...

Intuitively, it may seem unlikely that mere fasting could have any beneficial effect on degenerative neurological disease, but a recent study in a mouse model of Charcot–Marie–Tooth disease showed that intermittent fasting increases autophagy in Schwann cells in the PNS, reducing protein aggregation in these cells and increasing the thickness of myelin sheath (Madorsky et al., 2009).

Remarkably, the mice also showed improved locomotor performance, indicating that fasting can confer clinically evident benefits in a genetic neurodegenerative disorder (Madorsky et al., 2009).

Recently, we have ... demonstrated that brief (24–48 h) food restriction can induce neuronal autophagy in the brain; compared with normal-fed mice, the abundance of autophagosomes increases by three- to four-fold after 48 h of food restriction (Alirezaei et al., 2010).

____________________end quotes


But don't get too excited about fasting for 24-48h and get the same results. Mice are not little furry men with tails. Their metabolism is ~7-8 times faster than human. To help you get the idea, consider that a mouse eats about 25% of its weight daily and looses 10% of its weight after 24h of complete food deprivation. It looses 20% of its weight after 48h. For a non-obese man it will take 7-9 days to loose 10% of his weight, and more than 3 weeks to loose 20%. Of course, weight is not an issue here. This is just to show you the differences in murine and human metabolisms. There is another paper that showed that it takes about 7-8 days for a human, fasting on water only, to reach the same metabolic markers as a 40%-calorie-restricted mouse. So, it's important to keep these differences in mind when applying the research on mice to humans. The authors of this paper don't seem to be aware of this either.


This is the only time I jump your hoops here. It goes against my principles. I don't do "workarounds". So, whoever decided that my post about fasting was a spam, may want to adjust their trigger happy button pushing, or you people here will rob yourselves of valuable info that may help you more than you know. Is it so difficult to simply delete spam after it happens? Or it offends you so that you prefer to treat a priori all your guests as spammers? 


 My apologies to MunchMan for derailing his thread to fasting! I just noticed his nick, lol

That paper takes the conventional point of view that diseases such as MS are autoimmune, so the things it thinks would be a good idea might actually be the reverse of what one wants when fighting an infection. (Not that the paper makes strong statements either way; it's mostly a bland summary.)

Several medications are absorbed better while fasting (but this effect is probably marked also with more temporary fasting, and can be enhanced by physical activity -- at least for some medications). I discussed it previously, and it is also applicable to Metronidazole

Worth to note is that fasting hampers physical activity ability. Physical activity has numerous health benefits, and the higher the intensity, the more impressive the benefits. Diets high in complex carbohydrates have been found to have effects perceived as beneficial, e g Miller et al: Comparative Effects of 3 Popular Diets on Lipids, Endothelial Function and C-Reactive Protein during Weight Maintenance .


Borrelia/Cpn arthritis: joint, skin, eye, CNS, respiratory, UG involvment; fatigue. Borrelia Elisa&WB IgG, and CPn IgG and IgA pos, HLA-B27 neg. CAP 5/9/2010 -> 3/2016 2017: some signs and symptoms returning, Borrelia?

The sort of fasting we're discussing in this thread is a different thing from the "fasting" usually invoked in results for medication absorption: this fasting is extended lack of food, not eating for upwards of (say) 18 hours, while for fast medication absorption the requirement is only that the medications be taken "on an empty stomach".

Norman, yes, that's why I wrote "temporary fasting" (though, some studies of pharmacokinetics do have rather extended fasting to make resuts more clear-cut, so I recall both varieties are seen in such studies). It was actually much your experiences with Flagyl while fasting that you mention further up in this thread that I thought about (great thread and post, thanks!). Too often, the effect of food intake is downplayed, in my view. This can account for some effects of fasting (the effect on drug absorption is very likely there even in extended fasting while on medication, even if some studies on phramacokinetics are on "empty stomach" kind of fasting -- the effect is likely larger with extended fasting compared to "empty stomach"). 

The drawbacks I refer to in the second paragraph refers to the kind of fasting that is the main topic in this thread.

I guess I muddled up my post a bot by talking about both kinds of fasting and different effects.Image removed.

Borrelia/Cpn arthritis: joint, skin, eye, CNS, respiratory, UG involvment; fatigue. Borrelia Elisa&WB IgG, and CPn IgG and IgA pos, HLA-B27 neg. CAP 5/9/2010 -> 3/2016 2017: some signs and symptoms returning, Borrelia?

Hi nord, thanks for joining the discussion. Maybe mods could make the relevant portion of this thread into a topic of fasting? Otherwise it's off topic in Munchman's log.

Yes, the fasting I refer to is longer than 4-5 days (no food at all). That's the bare minimum to reach the metabolic markers when "magic" of fasting becomes noticeable. Even though I saw posts by people who only fasted 36h once a week and claimed that all of their chronic health problems went away after a year of such practice.

Norman, re paper, it has two parts, one pertaining AIDS, which is indisputably an infectious disease, and another MS, which, of course, this paper did not argue to be of infectious etiology. Such "revolutionary" claim would need an article of its own and not be buried in some review of autophagy and its role in immunity and health. I thought you could make this leap yourself and apply his arguments in regard to AIDS to MS. The interesting part is the references to research elucidating how intracellular infections dysregulate autophagy. Cpn, being an intracellular parasite, does it too, wouldn't you think?

Its best part, of course, is how fasting increased the thickness of myelini sheath in mouse model of MS.

The stuff about HIV in that paper is indeed transferrable to other pathogens, because the paper indicates that it's not some special HIV effect, but rather that inflammation in general downregulates autophagy. However, their language "we propose that, in infectious neurodegenerative diseases, some of the deleterious changes may result from the inhibition of neuronal autophagy" is a far cry from saying that "this is the key thing that goes wrong, and fasting can fix it". It's just a "proposal", not something they actually know for sure; and even then it only is about "some" of the effects of the infection, not all or even a majority. Furthermore, they're talking about mitigating effects of the infection, not about killing the causative pathogens, which is the really important thing.

Also, what the paper says about autophagy in the brain, during fasting, is that they needed a specially sensitive technique to find any increase in it; less sensitive techniques didn't find any. Indeed, it would be quite surprising if the brain shrank as much as fat and muscle does, during fasting; people diet to take pounds off their midsections, not to shrink their brains. They don't mention any experiments which might show whether the increase in autophagy that they found would persist in the presence of inflammation.

By the way, the increase in myelin sheath thickness was in a mouse model of Charcot-Marie-Tooth disease, not in a mouse model of MS. The two are very different diseases.