lassesen 9:15 pm on September 30, 2017

Paleo-ketogenic Diet for CFS – a good fit?

In my last few posts I looked at illnesses in the autoimmune spectrum that have started to have their microbiome studied. For each of them I used DataPunk.net to filter out good and bad things for correcting the shifts done. I then spot checked some of the things against the literature and discovered that the predictions of what could happen — frequently was found to help. The oddest one was that using diet-pop (versus regular pop) reduced the risk of Rheumatoid Arthritis was confirmed and matched the prediction that sugar substitutes helped correct/prevent this specific microbiome shift.

At present I do believe that CFS is likely a mixture of different microbiome shift patterns. This comes from two things:

the definition requires X of Y symptoms and symptoms are related to the microbiome shifts
going thru many uBiome results — I see the commonality of low or no lactobacillus, bifidobacterium and e.coli (originally reported in 1998) but with all of the other bacteria genus being all over the place.

We can shift microbiome patterns by diet. The problem is that the diet should match the microbiome shift desired. This means that any specific diet as a general recommendation to CFS patients becomes suspect without a detail examination of the microbiome first. Eating Navy beans and barley oatmeal for breakfast will help some and hurt others.

A reader asked explicitly about the paleo-ketogenic diet, so I will start by summarizing what research reports.

Paleo-ketogenic diet Research

Google Trends shows us that it started around 2009 and has been growing in interest.

google

Going to PubMed – Nothing for this search term. On Google Scholar, we had 681 hits (often blog posts). I used the following from the Ancestral Health Society’s “Annual symposium of the German Society for Paleo Nutrition”

http://jevohealth.com/journal/vol1/iss1/5/ (2013)
http://jevohealth.com/journal/vol1/iss1/6/ (2014)
http://jevohealth.com/journal/vol1/iss1/8/ (2015)

With the following being asserted:

“Adjusting to the ketogenic Paleo diet led to subjectively noticeable health benefits:
• Significant weight loss of 70 kg (154 pounds) within 15 months
• Enhanced metabolic fat burning and gains of lean body mass
• Improved cognitive performance
• Stronger immune system
• Mental balance and general well-being” 2013, p7

Bottom line, I was unable to find any clinical studies.

What is the diet and how does it impact the microbiome?

The ketogenic diet is a high-fat, adequate-protein, low-carbohydrate diet [Wikipedia]
The Paleolithic diet (also called the paleo diet, caveman diet or stone-age diet^[1]) is a modern fad diet requiring the sole or predominant consumption of foods presumed to have been the only foods either available or consumed by humans during the Paleolithic era [wikipedia]
- “the diet typically includes vegetables, fruits, nuts, roots, and meat while excluding foods such as dairy products, grains, sugar, legumes, processed oils, salt, and alcohol or coffee.^[1] The diet is based on avoiding not just modern processed foods, but rather the foods that humans began eating after the Neolithic Revolution when humans transitioned from hunter-gatherer lifestyles to settled agriculture.”

The wikipedia definitions actually provide us with sufficient information to infer what expected shifts in the microbiome may be due to our friend, DataPunk.Net.

Ketogenic Diet – simply BAD for CFS

A quick trip to DataPunk.net revealed that it inhibits Lactobacillus and double inhibits Bifidobacterium. Forget all of the other bacteria genus — it’s wrong for the basics!!!!

Enhances	Inhibits
High Fat	High Fat	low-carbohydrate
Alistipes	Actinobacteria	Agathobacter rectalis
Clostridium perfringens	Akkermansia	Bifidobacterium
Enterococcus	Akkermansia muciniphila	Prevotella
Erysipelotrichia	Bifidobacteriaceae	Roseburia
Fusobacterium	Bifidobacterium
Lactobacillales	Bifidobacterium pseudolongum
Proteobacteria	Clostridiales
Verrucomicrobiales	Clostridium clostridioforme
	Coprococcus
	Faecalibacterium
	Lactobacillus
	Lactococcus
	Ruminococcus
	Verrucomicrobia

Addenum:

UPDATE: I just checked the old CfsFMExperimental Group on Yahoo and the use of ketogenic diet was a topic on that group back in 2000-2005. It never went anywhere — although people tried it.

Paleolithic diet

High fruit intake: Enhances Alistipes
Plant Rich Diet: Inhibits Alistipes
Almonds/ almond skins: Enhances Bifidobacterium, Lactobacillus
Walnuts:
- Enhances: Bacilli Coprococcus Firmicutes Lachnospiraceae Lactobacillus reuteri Oscillospira Peptococcaceae Roseburia Ruminococcaceae Streptophyta Turicibacter
- Inhibits:Alphaproteobacteria Anaeroplasmatales Anaerotruncus Bacteroides Bacteroidetes Blautia Carnobacteriaceae Dehalobacter Erysipelotrichia Gammaproteobacteria Proteobacteria Tenericutes
High animal protein diet
- Enhances: Bilophila Bilophila wadsworthia
- Inhibits: Agathobacter rectalis Faecalibacterium Faecalibacterium prausnitzii Roseburia Ruminococcus bromii

Sesame seed: Enhances Bifidobacterium Enterococcus Lactobacillus

Compared to the ketogenic diet, the Paleolithic diet is a winner. Lean animal meat is in keeping with paleolithic life (all animals were wild and hunted by men and other creatures).

Bottom Line

I prefer a diet custom tuned to the microbiome shifts — but if you want a ‘stock diet’ I would prefer you to consider a paleolithic diet (although it is vaguely defined).

Remy 12:51 am on October 1, 2017

I’m having a lot of trouble with the idea of dispensing with the ketogenic diet entirely based on observed changes to the gut microbiome. It’s true that a ketogenic diet will change the gut microbiome (often drastically) but that is not necessarily a bad thing. In fact, it really might be a good thing. Only time will tell. We don’t really know what optimal is right now as the science in this area is constantly evolving. It’s one thing to say that healthy controls show one profile in the gut microbiome, but it’s completely illogical to extrapolate wildly from that and come to a conclusion that a ketogenic diet is “simply bad” for the microbiome. There is no research that shows that. The truth is that a ketogenic diet has MANY benefits for MECFS and other metabolic and neurological diseases. There is a lot of solid research evidence to support this statement that has been clearly overlooked here in the sole pursuit of increasing lactobacillus and bifidobacterium. For example, ketogenic diets provide 30% more energy over glucose metabolism. 30% more energy is a significant difference for most people with MECFS. Beyond that, a ketogenic diet is proven to increase mitochondrial function substantially and reduces systemic levels of inflammation, including in the brain. It has also been shown to promote hormone balance, increase brain clarity and cognition, reduce seizures and migraines, and promote muscle gain and endurance. Further, a ketogenic diet helps to improve sleep. Focusing on a lack of gut bacteria that are only required to degrade undigested carbohydrate (and thus are completely useless on keto) means absolutely nothing in terms of the many benefits of the ketogenic diet. It is the easiest, most profound way for someone to make meaningful long-lasting changes in their health without any doctor or medication required.
- lassesen 2:44 am on October 1, 2017
  
  UPDATE: I just checked the old CfsFMExperimental Group on Yahoo and the use of ketogenic diet was a topic there back in 2000-2005. It never went anywhere — although people tried it.
  
  The purpose of this blog is to be evidence based, or at least evidence supported.
  There are no studies on fibromyalgia using ketogenic diet, irritable bowel syndrome ketogenic diet or chronic fatigue syndrome ketogenic diet. It is effective for some conditions – for example, epilepsy. The ketogenic diet has been around since the 1970’s
  
  You cite a lot of true facts BUT for other conditions. NONE for CFS. That is the problem… that applies to other conditions. “30% more energy is a significant difference for most people with MECFS. ” is pure speculation — show me the study!!!!
  
  “No studies have been done on the effects of ketogenic diets in Chronic fatigue syndrome. Some CFS clinicians recommend ketogenic diets as a management strategy citing mitochondrial dysfunction, immune dysfunction, and neuroinflammation as pathways through which ketogenic diets could confer some benefit.” http://me-pedia.org/wiki/Ketogenic_diet — so it has been tried…. and no papers(or conference presentations as far as I could tell) from come out of clinical experience. All of the CFS MD’s state they are hypothesising that it could help. See http://www.medical-hypotheses.com/article/S0306-9877(15)00318-7/fulltext
  
  It may well help a percentage of CFS patients… but may also hurt a far greater percentage.
  
  IMHO, speculating that it will help because it vaguely helps metabolic functions without drilling into the specific mechanism is less founded than something that will also help metabolic functions and should shift the production of metabolites closer to normal be reducing specific over producing and encouraging specific under producers (with studies supporting those shifts)
  
  I am just advocating that the Paleo is a diet that is more probable to help.
  - Remy 9:58 pm on November 5, 2017
    
    IMHO, speculating that it will help because it vaguely helps metabolic functions
    
    You cite a lot of true facts BUT for other conditions. NONE for CFS.
    
    That’s true…but you do the same thing in your blog post on Suramin by using the research data for another similar drug. That’s what we do when the evidence is limited. We extrapolate from what is known and work from there. You don’t get to have it both ways.
    
    IMHO, speculating that it will help because it vaguely helps metabolic functions
    
    The data on how the ketogenic diet works is well documented. It’s not at all vague or particularly speculative. It is multifactorial, though, in many conditions that parallel the known defects in MECFS.
    
    It’s well accepted the ketones are more efficient than glucose in people in general, not for any one disease state and not for another. That means more energy, up to 30%, according to Dr Richard Veech who has studied the TCA cycle since he worked in the lab of a certain Krebs.
    
    This is particularly relevant in hypoxic states which also directly pertains to ME/CFS (Bell, Light’s, Shungu). Ketones are protective against hypoxia, full stop. https://www.ncbi.nlm.nih.gov/pubmed/6422588
    
    Beyond that, if one subscribes to the theory of Fluge and Mella regarding the potential block at pyruvate dehydrogenase, a ketogenic diet has also been shown to be of great benefit by providing a alternative work around for energy production. “A block in pyruvate dehydrogenase decreases citrate concentrations, the precursor of acetyl choline,through the action of citrate cleavage enzyme(EC 4.1.3.8)andcholine acetyl transferase(EC 2.1.3.8). Metabolism of ketones overcomes the decrease in citrate content. It has now been shownthat when cultured hippocampal neurons are exposed to A¯1¡42, they die. Addition of 4 mMD-B-hydroxybutyrate protected these neurons from A¯1¡42 induced death(25).” http://onlinelibrary.wiley.com/doi/10.1080/152165401753311780/epdf
    
    So, in a nutshell, there’s no good evidence for a negative effect on the microbiome and there is robust evidence for the increased energy, decreased brain fog, neuroprotective ketogenic diet. Ketogenic diets, even the crappy ones used in early epilepsy studies, show no evidence of long term harm…to anyone.
    - lassesen 2:30 pm on November 6, 2017
      
      Absolutely agreed on the “Studies not for CFS” — that’s the problem there are none. Given the diversity of microbiome seen in CFS as well as diversity of symptoms — we are talking a study size of at least 1000. My proxy is simple, impact on microbiome — and I call out that it is best to decide once you know your personal microbiome shift. It’s not perfect, but it does follow a logical pattern
      - Catherine 2:56 am on December 3, 2017
        
        Ken,
        
        Am I in one of those jigsaw puzzle phases?
        
        You have advocated that we now have the ability to look at our own bacteria profile and find a treatment mix tailored for each of us. You have also throughout your website have said that one of the vexing problems of treating CFS, FM, etc is that nothing works for all. With that in mind the highest offending bacteria genus for my daughter is erysipelatoclostridium (4.43X). Your summary page on decreasing it cites a study where the Ketogenic diet was effective in reducing it:
        “ketogenic diet exposure also induced a decrease in Erysipelatoclostridium (by 8.67% ..)” [2017]
        We have just gotten her biome profile and have been charting out how we want to proceed based on your ‘How to decrease….’ links. Yet above you caution against doing the ketogenic diet in part because it inhibits the way it impacts certain bacteria.
        Would my daughter potentially be one of the sufferers who could benefit from a Ketogenic diet?
        
        Thanks,
        Catherine
        
        lassesen 9:41 pm on December 3, 2017
        
        Welcome to the world of doing fuzzy analysis with only fragments of information to work from! (Unfortunately).
        
        My suggestion is to see how many of your high genus are on the Enhances and Inhibits ones listed above. If you have more on the Enhances list then avoid. If you have more on the Inhibits list, then try it. It is a very rough algorithm to apply, but with no more information(studies) to work from, it is likely the best that we can do.
Jalno 11:36 am on December 20, 2017

I have cfs, but my bowel function is perfect. Every morning and consistent.
I cant see how altering microbiome can affect a metabolic condition, especially when ones’ digestive system is running like textbook.
CFS is a metabolic oxphos shutdown to protect cell from threat. Much like having a permanent flu in a low grade way. Normal people shut down in flu to protect organism, pity about CFS its stays on high alert post trauma. Ketosis (and high dose amino) works because body has shut down glycosis pathway. Prehaps the connection from gut to immune system will unveil itself in due course, but for now, we have to address symptoms, (fatigue, malaise, PEM) through metabolic means, not gut means.
- lassesen 4:36 pm on December 20, 2017
  
  During my 1st and 2nd CFS episode I would have agree with you.
  The only real test would be to have your uBiome done – you may have a major shift and be asymptomatic for gut issues …. if your ubiome is normal, you become an interesting case and very atypical from several dozen CFS ubiomes that I have reviewed.
  
  Which symptoms listed at: https://cfsremission.com/2017/12/17/list-of-common-cfs-symptoms-whats-missing/ do you have?
Susan McIntyre 4:11 pm on May 20, 2018

Hello,

This airborne pathogen gave me symptoms of Fibromyalgia. Can it cause CFS? I’d like to share information I learned during my workplace’s outbreak of an underdiagnosed airborne infectious disease that can cause malignancies, precancerous conditions, rheumatological diseases, connective tissue diseases, heart disease, autoimmune symptoms, inflammation in any organ/tissue, adrenal insuffiency, seizures, migraines, mood swings, hallucinations, etc. and is often undiagnosed/misdiagnosed in immunocompetent people. 80-90+% of people in some areas have been infected, and it can lay dormant for up to 40 years in the lungs and/or adrenals.

My coworkers and I, all immunocompetent, got Disseminated Histoplasmosis in Dallas-Fort Worth from roosting Mexican Free-tailed bats, the most numerous non-human mammal in the U.S., that shed the fungus in their feces. The doctors said we couldn’t possibly have it, since we all had intact immune systems. The doctors were wrong. Healthy people can get it, too. And we did not develop immunity over time. We’d get better and then progressively worse, relapsing periodically and concurrently every year.

More than 100 outbreaks have occurred in the U.S. since 1938, and those are just the ones that were figured out, since people go to different doctors. One outbreak was over 100,000 victims in Indianapolis.

It’s known to cause hematological malignancies, and some doctors claim their leukemia patients go into remission when given antifungal. My friend in another state who died from lupus lived across the street from a bat colony. An acquaintance with alopecia universalis and whose mother had degenerative brain disorder has bat houses on their property.

Researchers claim the subacute type is more common than believed. It’s known to at least “mimic” autoimmune diseases and cancer and known to give false-positives in PET scans. But no one diagnosed with an autoimmune disease or cancer is screened for it. In fact, at least one NIH paper states explicitly that all patients diagnosed with sarcoidosis be tested for it, but most, if not all, are not. Other doctors are claiming sarcoidosis IS disseminated histoplasmosis.

What if this infection, that made me and my coworkers so ill, isn’t rare in immunocompetent people? What if just the diagnosis is rare, since most doctors apparently ignore it? Especially since online documents erroneously state it’s not zoonotic.

Older documents state people who spend a lot of time in a building with roosting bats, in caves, working as landscapers, construction workers, pest control workers, etc. are known to get Disseminated Histoplasmosis, but the info appears to have been lost, for the most part. And now bat conservationists encourage people to leave bats in buildings/homes. What a terrible mistake they’ve made.

This pathogen parasitizes the reticuloendothelial system/invades macrophages, can infect and affect the lymphatic system and all tissues/organs, causes inflammation, granulomas, and idiopathic (unknown cause) diseases and conditions, including hematological malignancies, autoimmune symptoms, myelitis, myositis, vasculitis, panniculitis, dysplasia, hyperplasia, etc. It causes hypervascularization, calcifications, sclerosis, fibrosis, necrosis, eosinophilia, leukopenia, anemia, neutrophilia, pancytopenia, thrombocytopenia, hypoglycemia, cysts, abscesses, polyps, stenosis, perforations, GI problems, hepatitis, focal neurologic deficits, etc.

Many diseases it might cause are comorbid with other diseases it might cause, for example depression/anxiety/MS linked to Crohn’s.

The fungus is an Oxygenale and therefore consumes collagen. It’s known to cause connective tissue diseases (Myxomatous degeneration?), rheumatological conditions, seizures, and mental illness. Fungal hyphae carry an electrical charge and align under a current. It causes RNA/DNA damage. It’s known to cause delusions, wild mood swings (pseudobulbar affect?), and hallucinations. It’s most potent in female lactating bats, because the fungus likes sugar (lactose) and nitrogen (amino acids, protein, neurotransmitters?), releasing lactase and proteinases to obtain them. What about female lactating humans…postpartum psychosis (and don’t some of these poor women also have trouble swallowing)? The bats give birth late spring/summer, and I noticed suicide rates spike in late spring/early summer. It’s known to cause retinal detachment, and retinal detachments are known to peak around June-July/in hot weather. A map of mental distress and some diseases appear to almost perfectly overlay a map of Histoplasmosis. Johns Hopkins linked autism to an immune response in the womb. Alzheimer’s was linked to hypoglycemia, which can be caused by chronic CNS histoplasmosis. Cancer is known to occur more often near rivers than in mountains or deserts, just like this infection. The bats eat moths, which are attracted to blue and white city lights that simulate the moon the moths use to navigate. Bats feed up to 500 feet in the air and six miles away in any direction from their roost, but not when it’s raining or when the temperature is less than approximately 56° F. The fungus can grow in bird feces, but birds don’t carry it because their body temperature is too high, killing the fungus.

I believe the “side effects” of Haldol (leukopenia and MS symptoms) might not always be side effects but just more symptoms of Disseminated Histoplasmosis, since it causes leukopenia and MS symptoms. What about the unknown reason why beta receptor blockers cause tardive dyskinesia? The tinnitus, photophobia, psychosis “caused” by Cipro? Hypersexuality and leukemia “caused” by Abilify? Humira linked to lymphoma, leukemia and melanoma in children? Disseminated Histoplasmosis is known to cause enteropathy, so could some people thought to have nonsteroidal anti-inflammatory drug enteropathy have it and taking NSAIDs for the pain/inflammation it causes, and the NSAIDs aren’t the actual culprit?

From my experience, I learned that NO doctor, at least in DFW, will suspect subacute and/or progressive disseminated histoplasmosis in immunocompetent people. Some doctors, at least the ones I went to, will actually REFUSE to test for it, even when told someone and their coworkers have all the symptoms and spend a lot of time in a building with bats in the ceiling. Victims will be accused of hypochondriasis. (My doctors told me only farmer’s get it, it’s only in bird feces, and it only infects the lungs…wrong, wrong, and wrong!) In fact, the first doctor to diagnose me was a pulmonologist, and the only reason he examined me was to try to prove that I didn’t have it, when I really did. No doctor I went to realized bats carry the fungus. And NO doctor I went to in DFW, even infectious disease “experts,” understand the DISSEMINATED form, just the pulmonary form, and the only test that will be done by many doctors before they diagnose people as NOT having it is an X-ray, even though at least 40-70% of victims will have NO sign of it on a lung X-ray. It OFTEN gives false-negatives in lab tests (some people are correctly diagnosed only during an autopsy after obtaining negative test results) and cultures may not show growth until after 6-12 weeks of incubation (but some labs report results after 2 weeks).

One disease of unknown cause that could be caused by Disseminated Histoplasmosis: I suspect, based on my and my coworker’s symptoms (during our “rare” infectious disease outbreak) and my research, that interstitial cystitis and its comorbid conditions can be caused by disseminated histoplasmosis, which causes inflammation throughout the body, causes “autoimmune” symptoms, and is not as rare as believed. I read that “interstitial cystitis (IC) is a chronic inflammatory condition of the submucosal and muscular layers of the bladder, and the cause is currently unknown. Some people with IC have been diagnosed with other conditions such as irritable bowel syndrome (IBS), fibromyalgia, chronic fatigue syndrome, allergies, and Sjogren’s syndrome, which raises the possibility that interstitial cystitis may be caused by mechanisms that cause these other conditions. In addition, men with IC are frequently diagnosed as having chronic nonbacterial prostatitis, and there is an extensive overlap of symptoms and treatment between the two conditions, leading researchers to posit that the conditions may share the same etiology and pathology.” Sounds like Disseminated Histoplasmosis, doesn’t it?

My coworkers and I were always most ill around April/May/June, presumably since the Mexican Free-tail bats gave birth in Texas during May (and the fungus was most potent), and fall/Thanksgiving to December, for some unknown reason (maybe migrating bats from the north?). We had GI problems, liver problems, weird rashes (erythema nodosum, erythema multiforme, erythema marginatum/annulare, etc.), plantar fasciitis, etc., and I had swollen lymph nodes, hives, lesions, abdominal aura, and started getting migraines and plantar fasciitis in the building, and I haven’t had them since I left. It gave me temporary fecal incontinence, seizures, dark blood from my intestines, tinnitus, nystagmus, blurry viion/floaters/flashes of light, benign paroxysmal positional vertigo, isolated diastolic hypertension, what felt like burning skin, various aches and pains (some felt like pin pricks and pinches), tingling, tremors, “explosions” like fireworks in my head while sleeping, temporary blindness, and chronic spontaneous “orgasms”/convulsions. Suddenly I was allergic to Comice pears (latex fruit allergy or oral allergy syndrome?). I had insomnia (presumably from the fungus acidifying the blood, releasing adrenaline) and parasomnias. It felt like strong bursts of eletrical shocks or stady electrical currents in my body, which now feel like low electrical currents at times, mostly at night. I suddenly had symptoms of several inflammatory/autoimmune diseases, including Fibromyalgia, Sarcoidosis, ALS, MS, Sjogren’s syndrome, etc. that have disappeared since leaving the area and taking nothing but Itraconazole antifungal.

No one, including doctors (we all went to different ones), could figure out what was wrong with us, and I was being killed by my doctor, who mistakenly refused to believe I had it and gave me progressively higher and higher doses of Prednisone (at least 2 years after I already had Disseminated Histoplasmosis) after a positive ANA titer, until I miraculously remembered that a visiting man once told my elementary school class that bats CARRY histoplasmosis….so much of it that they evolved to deal with the photophobia and tinnitus it causes by hunting at night by echolocation. There’s a lot more. I wrote a book about my experience with Disseminated Histoplasmosis called “Batsh#t Crazy,” because bats shed the fungus in their feces and it causes delusions and hallucinations, I suspect by the sclerotia fungal mycelia can form emitting hallucinogens (like psilocybin and dimethyltryptamine) along with inflammation in the CNS. (Schizophrenics have 2X of a chemical associated with yeast, part of the fungal life cycle.)

Thank you for your time,

Susan McIntyre

P.S. Doesn’t this infection share all the same symptoms with Gulf War Syndrome?
- lassesen 8:39 pm on May 20, 2018
  
  This is compatible with my model. The key aspect is that the triggering event may not be the sustaining event/cause. I would love you to try getting several (ideally 6 or more) of fellow sufferers get their uBiome done to see if there is a shared pattern of microbiome shift.
  
  Ubiome.com did announce a ubiome Explorer Plus which include fungal signatures. They do not appear to have started shipping them.
Lea Milgraum 6:10 pm on December 11, 2021

You might want to look at Dr Myhill’s work on CFS and Pale-ketogenic diet. She has extensive experience and success with it.
- lassesen 5:37 am on December 12, 2021
  
  This is an old post. Today, with a 16s microbiome sample, we can better predict whether it will help or hurt.
  
  The impacts are better known:
  see https://microbiomeprescription.com/library/modifier?mid2=215
Ruth Davies 5:20 pm on August 8, 2022

Oh wow, I have got to say, I geeked out on this whole debate.