Wednesday, September 26, 2012

Is ME/CFS an mental illness – an comment

I made an comment at an (otherwise not noteworthy) article:
Three researchers – Mikovits, Ruscetti and Lombardi – published one (possibly fraudulent) study, a study that didn't help up to scrutiny – that doesn't mean that ME/CFS is an mental illness.

You should look into the work of Alan Light, a Research Professor of Anesthesiology at the University of Utah.

His topics are:
- Cellular Neuroscience
- Neurobiology of Disease
- Molecular Neuroscience
- Brain and Behavior

He has done some research into pain (and now fatigue) of – among other diseases – ME/CFS. His work shows differential gene expression in peripheral blood cells of ME/CFS patients after an exercise challenge – this indicates increase pain and fatigue in sensory nerve endings at the muscle level.

Two of his lectures (available on YouTube) are in my view recommendable to come up to speed to his research:

2007 Lecture: "The Physiology of Chronic Pain and Fatigue"

2011 Lecture: "Gene Expression Biomarkers for Chronic Fatigue & Fibromyalgia Syndromes"

In my opinion the findings by Alan Light rule out mental illness as an probable disease model for ME/CFS.
[I reworked the comment slightly for this blog]

Sunday, September 23, 2012

How to take idealistic psychosomatic bollocks apart

Burning Mouth Syndrome

Psychologic Dysfunction

Personality and mood changes (especially anxiety and depression) have been consistently demonstrated in patients with burning mouth syndrome and have been used to suggest that the disorder is a psychogenic problem.

However, psychologic dysfunction is common in patients with chronic pain and may be the result of the pain rather than its cause.

The reported success of biobehavioral techniques in the treatment of burning mouth syndrome may be related more to an improvement in pain-coping strategies than to a “cure” of the disorder.

Similarly, the usefulness of tricyclic antidepressants and some benzodiazepines may be more closely related to their analgesic and anticonvulsant properties, and to the possible effect of benzodiazepines on taste-pain pathways.
Just four sentences to show what a load of bollocks the idealistic "psychosomatic" model of diseases is – and that nothing in biology makes senses except in the view that we live in a materialistic world, not an idealistic world (to paraphrase Dobzhansky's remark about the "light of evolution").

Dairy and that Sore Mouth Feeling

So, having not eating dairy for quite some time now, I recently started trying out cheese again. And trying only cheeses made from raw-milk. My focus was if I get ill health effects, especially acne. And what can I say, raw-milk cheese does not cause acne for me – unlike cheese from pasteurized milk, which does cause acne for me. (And just for the record: I had no repeat of an hypoglycemia episode.)

But now I noticed another effect of dairy: An slightly sore mouth immediately while I eat cheese, and especially in the palate. And I remember I had this feeling many time before, while I was eating certain cheeses. But I never really took much notice of it.

(And furthermore, now some eight hours later, I feel even one "canker sore" or "aphthous ulcer" appear, something I had in my pre-Paleo days)

I wouldn't go so far and describe my mouth sensation as a "burning" (so I guess it is not "burning mouth syndrome" or Glossodynia), but it sure does feel a slight bit "scalded".

Wikipedia (as an reflection of what is "known" in medical sciences) is funny:
Possible causes include nutritional deficiencies, chronic anxiety or depression, type 2 diabetes, menopause, oral disorders such as thrush or dry mouth, or damaged nerves (specifically, cranial nerves associated with taste).
So there seems to be a correlation between glossodynia and chronic anxiety, and between glossodynia  and depression. I would say: Is it possible that all three are caused by an as of now undetermined third factor? I would throw in milk as an educated guess. But wikipedia instead suggests that there is a causative relationship. What bollocks, IMHO, to think that depression could cause glossodynia. Oh well.

By now, if I read such a hodgepodge of associations and no clear etiology, I would always suggest trying out an Paleo style elimination diet (no cereal grains, no dairy, no vegetable oil, no "crap in a box" and no soy), to see if the condition improves. Then, if one can't live without the crap, one can reintroduce it slowly, one by one, to see who is the culprit. Or one could simply stay on a Paleo diet.

Saturday, September 22, 2012

Fat Head

Fat Head, a must-see documentary about diet myths.

Non-celiac wheat sensitivity?

I’ve long suspected that everyone has some degree of sensitivity to gluten, even if they’ve never been formally diagnosed and even if they don’t notice any overt symptoms after eating it. Now we have concrete evidence that non-celiac gluten sensitivity actually exists. My own story was that of a lifetime grain-eater who defended my “right” to eat grains until I was 47 – until the evidence was just too overwhelming to ignore. Once I gave them up as part of a 30-day experiment, lo and behold, my arthritis cleared up, my lifelong IBS went away, and my occasional GERD disappeared. Ditching grains, especially wheat, changed my life for forever and made me understand how easy it is for so many people to overlook this possible problem.

A recent study … confirmed the existence of non-celiac wheat sensitivity. Subjects without the atrophied villi (tiny projects that line the intestines and help absorb nutrients) characteristic of celiac and without positive tests for various markers that indicate celiac experienced gluten-related symptoms after a blinded wheat challenge. It doesn’t give us much of a clue as to the prevalence of sensitivity, but it establishes that such a thing might exist among the general population.

It’s not even the only study. It’s just the latest of many to establish and/or hint that non-celiac gluten sensitivity exists:
  • “Spectrum of gluten-related disorders: consensus on new nomenclature and classification.” (2012)
  • “Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial.” (2011)
  • “Is gliadin really safe for non‐coeliac individuals? Production of interleukin 15 in biopsy culture from non‐coeliac individuals challenged with gliadin peptides.” (2007)
While I too suspect that there are more disesaes caused by cereal-grain than celiac disease alone, it seems all a bit murky still what other adverse health effects grains have – and especially what the mechanisms are.

We'll see. But it is always nice to see that Mark has gathered together some studies for the topic.

The occurrence of Celiac Disease has increased in the US

Natural history of celiac disease autoimmunity in a USA cohort followed since 1974.

During a 15-year period CD prevalence increased 2-fold in the CLUE cohort and 5-fold overall in the US since 1974. The CLUE study demonstrated that this increase was due to an increasing number of subjects that lost the immunological tolerance to gluten in their adulthood.


Dear Jo Nijs,

I have a question regarding one of your results.

You state that:
"From the available literature, it is concluded that musculoskeletal factors are unlikely to account for pain from CFS."

My question originates from the 2009 study "Light AR, White AT, Hughen RW, Light KC. Moderate exercise increases expression for sensory, adrenergic, and immune genes in chronic fatigue syndrome patients but not in normal subjects." that you cite in your paper.

I was under the impression that the data by the author Alan Light actually suggest that it are the sensory nerve endings on the muscles that sense increased fatigue (and in extension pain) in CFS (and Fibromyalgia).

E.g. as Alan Light says here in a lecture (at minute 4:11):

I would like to ask what suggest that the increased expression of sensory genes in peripheral blood cells is a phenomenon occurring centrally, and what makes you think that changes in peripheral blood are a central phenomenon and therefore "unlikely" to originate from musculoskeletal factors.

Kindest regards
I really had to watch my language with such fine research from such fine researchers.

A prediction for ME/CFS

Here's my prediction for what Lipkin will find in ME/CFS patients (take it with some grains of salt):
  • He will find two dominant distinct diseases in roughly 60% of patients: One disease will have an share of about 40% of patients, while the other will be about 20%.

    The two dominant diseases he will find will be either: in the form of an "new" autoimmune disease (as of now undocumented autoimmune-antibody/antigen and target tissue), or an undocumented presentation of a known virus (e.g. one of the HHVs or Enteroviruses), or an combination thereof.

    An unknown virus is possible, but seems to me unlikely.
  • About 25% of patients will be comprised of patients with on of about 10 diseases. Diseases will be e.g. atypical presentations of known common diseases, and possibly some novel diseases.
  • The remaining 15% of patients will have a multitude of diseases, some common and some rare, some known and some currently unknown.
The great unknown seems to be the role of HHVs. Interesting will be whether the majority of patients have an "simple" disease (e.g. with one autoimmune-antibody targeting one tissue type as prime cause) that "simply" causes the complex "multi-organ" disease presentation, or whether there is actually multi-organ involvement as prime cause.

Let's see – I'm not taking bets.

Friday, September 21, 2012

Imagine ME/CFS without Ian Lipkin

So, what would have been the state of ME/CFS without Ian Lipkin:
  • Mikovits would have continued to insist "IT IS XMRV / MLV / pMLV / HGRV !!!!!!!!!"
  • A sizable portion of patients and "advocates" would have continued to insist "IT IS XMRV / MLV / pMLV / HGRV!!!!!!!!!"
  • Nobody would have believed the ME/CFS community ("It's all in the head, you know")
This would have been the mess, created by Mikovits (and Ruscetti) – hadn't Ian Lipkin stepped up.

Should I thank Mikovits for creating a mess?

Mikovits effectively hijacked large parts of the ME/CFS community, and tried to drive us down the XMRV dead-end.

Should I thank Mikovits for chasing us down the XMRV dead-end?

Mikovits convinced some patients to take anti-retroviral medications against viruses that they didn't had. What harm did that? What side effects did it cause? Was there permanent health damage for people taking medication that they didn't need? So was it only a "financial" loss? At least, as far as I know, nobody died from that. 

Should I thank Mikovits that she didn't kill anybody?

I'm grateful that Ian Lipkin got involed to clean up the mess created by Mikovits and Ruscetti.

Should I thank Mikovits and Ruscetti, that Lipkin cleaned up their mess?

And after all that, Mikovits hasn't managed to say one word in the way of an apology.

Should I thank Mikovits for not owing up to her deception?

Or should Mikovits and Ruscetti rather fear prison for their reckless behavior?

Wednesday, September 19, 2012

Another "Oldies, but Goodies" episode

Thanks to RRM for bringing this to the attention of us all.
Patrick Moore
March 6, 2011, 9:05 pm

Occam’s Razor of Virology: When you find a virus that causes disease, the disease should be easier to understand and not harder.

If you have to come up with more explanations for the virus than you would without it, then you are wrong (e.g., XMRV infection is not a HERV and is restricted to a rare form of prostate cancer and CFS–diseases which share no apparent common features. Somehow, these prostate cancer and CFS patients have a common exposure to this virus as a risk factor despite there being no common epidemiologic patterns. Although XMRV is clearly a murine ERV, people with exposure to mice are not at noticeable risk for prostate cancer or CFS).

It makes more sense that XMRV is a murine ERV that jumped to a human prostate cancer cell line decades ago when it was passaged through a nude mouse as a xenograft (a common practice) as elegantly shown by the Hue et al Retrovirology article. It has since been detected as an intermittent PCR contaminant.

My advice, above all else, is to test samples blindly and randomly. If you have PCR contamination, your results will be “biased toward the mean” of no significant relationship. This is the easiest and least costly confirmation possible. When your postulated virus-disease relationship survives this stringent test, then you possibly have something. Then, the science begins. Randomized and blinded testing has saved me, on multiple occasions, from appearing to be a bigger idiot than my natural talents for idiocy allow.

For what it is worth, when the CFS-XMRV paper was first published, we had severe concerns about its methodology and conclusions, which was published in F1000 (subscription required so it is reprinted below). I think it it is still valid:

Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome.
Lombardi VC, Ruscetti FW, …, Silverman RH, Mikovits JA
Science 2009 Oct 23 326(5952):585 -9 [abstract on PubMed] [full text]
DOI: 10.1126/science.1179052 PMID: 19815723
Competing interests: None declared


The discovery of the cause of chronic fatigue syndrome would be an extraordinary finding. Rather than providing extraordinary proof, this manuscript has flaws that leave the reader unsure of knowing precisely what was measured.

To detect the xenotropic murine leukemia-like virus (XMRV), the authors used nested-PCR on non-randomized and non-blinded samples, a recipe for uncontrolled PCR contamination. This technique re-amplifies previously cycled products and is inherently prone to intermittent false positivity that has occurred in our lab and many others (e.g. {1} and {2} on which I am the author). This is a concern in light of post-publication claims that XMRV detection rates among chronic fatigue syndrome (CFS) patients have climbed from 67% to 95%, and XMRV tests are now being sold and advertised on the internet at

Southern blotting, which would allay this suspicion, was not done. Other results in the study also lack support. Flow cytometry and immunostaining with murine leukemia virus (MLV) antibodies were used to directly detect viral proteins in patient cells (see Figure 2A of the paper). The CFS peripheral blood cells have robust monotonic staining rather than the bimodal peaks that are expected from a mixture of infected and uninfected populations of peripheral blood cells. It is not certain whether this level of viremia for an exogenous retrovirus is medically possible. It may, perhaps, be possible but it seems improbable and is a pattern more consistent with a cross-reactive endogenous retroviral antigen.

To confirm this finding, CFS peripheral blood cells (without negative controls in Figure 2B) were immunoblotted using cross-reactive spleen focus-forming virus (SFFV) and MLV antibodies. XMRV gp70 and p30 proteins are found at higher levels in 2 out of 5 CFS peripheral blood samples (1150 and 1221) than in the positive control — HCD-57 cells directly infected with SFFV — a very remarkable result. Repetition with negative control samples (see Figure 2C of the paper) has the higher molecular weight bands cut from the photograph, thus we cannot interpret potential positivity for p30 gag precursor proteins among the control samples (see CFS samples 1199 and 1220 in Figure 2B).

Finally, the positive control HCD-57 cell lane in Figure 2C lane 8 has a completely different banding pattern from the very same control in Figure 2B lane 7 for the p30 gag protein. The elementary issue of whether the authors are measuring XMRV has to be clarified. The fundamental basis for the CFS case and control samples is also not defined at an appropriate level. The samples (supplementary online material) were “selected for this study from patients fulfilling the 1994 CDC Fukuda Criteria for Chronic Fatigue Syndrome (S1) and the 2003 Canadian Consensus Criteria for Chronic Fatigue Syndrome/myalgic encephalomyelitis (CFS/ME) and presenting with severe disability”. These are two separate definitions, the latter published in the “Journal of Chronic Fatigue Syndrome” (which is no longer in print). It is unclear how the samples were selected from these two criteria. No references or cut-offs are given for tests used to clinically define the CFS patients as cases so we are unable to interpret the essential basis for the study. In addition, no description is given to indicate that controls were tested in the same manner as CFS patients; in fact, there is no description for negative control samples at all. For a disease whose diagnosis is controversial, a clear statement of where and how the cases and controls were selected is a critical first step.

"XMRV has never replicated outside of the laboratory setting."

XMRV has never replicated outside of the laboratory setting.
The association of XMRV with prostate cancer has now been thoroughly refuted.
So Silvermann does the right thing and tells us that there isn't XMRV in prostate cancer either – so this case is closed as well.

XMRV was from the beginning an dead end – no matter how much misinformation Mikovits and her acolytes have spread, with daily changing sock-puppets. Don't expect an apology from Mikovits, or Gerwyn/V99 and his army of sockpuppets, for chasing the ME/CFS community down an dead end.

The one thing that remains lacking is an truthful explanation by Mikovits and Ruscetti as to their "amazing" lab-results – what has been presented so far in the way of explanations remains inadequate.

Tuesday, September 18, 2012

Is Ruscetti an clever Schweinehund or what?

There were some positive results returned by the NCI-Cornell-Mikovits team using another method that looked for antibody reactions to these agents. Dr. Francis Ruscetti’s NCI lab tested serum from the coded samples using a flow cytometry-based assay slightly modified from the one he reported in the original 2009 Science paper. The team detected antibodies in human serum but when the code was broken, it revealed equal numbers of CFS cases and healthy controls had these antibodies – nine in each group, or six percent of the subjects. The paper states, “The serology results are more difficult to address given that the assay cannot be validated with plasma from humans with confirmed [???] XMRV or MLV infection. We posit that positive results represent either nonspecific or cross-reactive binding and note that irrespective of explanation, a positive signal does not correlate with case status.”
So he claims to use a "slightly modified" assay.

And results are indistinguishable if he had thrown in randomly some positive results.

Mmmm. Hmmm. Right.

How convenient for our dear Dr. Ruscetti, how convenient indeed.

And I can see our dear Dr. Ruscetti played it much cooler than our dear Dr. Mikovits. He is a much much cooler customer. Much much cooler indeed.

Sir, you played that nice and safely – chapeau.

Small sample sizes for the serology done in his lab. Ambiguity about whether the tests were done blinded. A few "false" positives mixed in. A nice signal, but enough noise (with the small sample size) so he has his bases covered.

If there had been actually an virus involved in ME/CFS, he could have claimed "We found it first!" – even if it had been some completely different virus.

And now he say with a straight face: "My bad – sorry."

A cool customer indeed. Plausible deniability and exit strategy, played like the real pro he is.

One can see that Dr. Francis Ruscetti has learned from our dear Dr. Robert Gallo, a master in his field.

And I guess John Crewdson would fully agree. Science Fictions indeed, now in their (at least) third generation.

Only Mikovits overplayed her hand, quite a bit I'd say. Not everybody is an natural talent like Ruscetti. One can see what Gallo liked in Ruscetti. And why Gallo fired Ruscetti – Ruscetti is simply a much cooler customer than Gallo. Gallo likes to overplay his hand, he needs to make it big – Ruscetti plays it much safer.

No XMRV means no more money for Ruscetti to pocket. And no money for Ruscetti to pocket means no Ruscetti. I say good riddance, with people like Ruscetti helping us to relieve us from urgently needed research money, with people like him we will go under while he stuffs his pockets.

Ruscetti has his bases covered and other than that keeps his lips tight.

Lombardi is tight lipped as well.

But it's Mikovits who has put her head above the parapet – she could very easily play the fall gal. And rightfully so, I would like to add.

As she doesn't want to play the fall gal, I wouldn't be surprised if she goes into blame-mode again, trying to throw somebody under the bus. Either she plays it straight (and we know that is not her style) and tries to shifts blame to Lombardi. Or she will go to full-retard mode and attempt to throw Lipkin under the bus – which wouldn't surprise me. Or she has gained some sense and plays it cool, keeping her lips shut.

We'll see, we'll see.

We have lost three years to this shit.

Three years.

Thankfully there is other research going on. And Ian Lipkin looking for answers is an real plus, an real asset.

I for one am not thankful for what Mikovits, Ruscetti and Lombardi did – their selfish actions could have easily destroyed most possibilites for progress in ME/CFS for at least the next decade.

Let's hope for the best, and prepare for the worst.

The XMRV-fraud is over! No MLVs or other related viruses in humans! Is the work of Mikovits and Ruscetti only sham?

So the "Multicenter study" by Ian Lipkin has announced its results:
[Mikovits and Ruscetti, among others] were wrong about a potential link between chronic fatigue syndrome and these viruses. 
I fully expect the Gerwyn/V99 sockpuppet army to ignore the findings by Ian Lipkin, and flood the comment sections to put their deluded and manipulative spin on things.

It's over. 

The XMRV-fraud is over! No MLVs or other related viruses could be found in humans.

There is no "HGRV", there is no XMRV infection in humans, there is not pMLV in humans, and there is certainly no MLV in humans.

You have been had.

The reported results from Mikovits and Ruscetti were riddled with inconsistencies and impossibilities. Whatever they reported, it was no real life process in humans.

It was not real, it was artificial.

The reported results were lab-artifacts, and furthermore lab-artifacts that can – in their total sum – rationally be only explained as intentional.

Mikovits was pushing a sham.

Everything Mikovits said had only one effect: To muddy the waters.

Not a single word written or uttered by Mikovits can be trusted.

It is sad that people fell for her and her deceptive words – we now have to move on from this mess created by Mikovits and Ruscetti.

Gerwyn/V99 and his sockpuppets are hacks.

I fully expect Gerwyn/V99 and all the other deluded acolytes to continue their self-deceptive promotion of BS instead of science.

Same as Mikovits, not a single word by this army of sockpuppets can trusted.

What will Mikovits say now?

I fully expect her to do some BS and try to throw someone under bus. What ever BS and sham was happening around her, she always blamed other people – I fully expect that pattern to continue.

Was it fraud by Mikovits and Ruscetti?

The legal definition of fraud is as follows:
A false representation of a matter of fact—whether by words or by conduct, by false or misleading allegations, or by concealment of what should have been disclosed—that deceives and is intended to deceive another so that the individual will act upon it to her or his legal injury.
We now know as an matter of fact that "XMRV/(p)MLV" are not involved in ME/CFE – claiming otherwise (as Mikovits did) was an false representation of an matter of fact.

The question whether Mikovits' behavior was fraudulent (or just plain stupid) rests on the question: Did Mikovits intend to deceive us?

It is always hard to look into brains of people – and especially with someone like Mikovits who muddies the water with every word she says.

But if pressed, I would say the actions and words of Judy Mikovits were intentional.

Monday, September 17, 2012

Vampire, meet Stake

The Lipkin study results will be announced soon. I dearly expect that Ian will drive a stake through the vampire-study, that study that has sucked out the blood from the ME/CFS community. And with all matters undead, if Ian does it not right, the Mikovits/Ruscetti-study will continue to haunt us.

And if Lipkin would actually find out something about ME/CFS – unlike the anti-science produced by the Ruscetti and Mikovits hacks – then that would be really dandy.

Wednesday, September 5, 2012

Diets: Atkins, Lutz, Low-Carb, Paleo, Ketogenic…

Attention conservation notice: I will focus in this post on the ketogenic diet, and whether it helped me (spoiler: it did not help me). I will try to focus on the other diets in some future posts, when I find the energy.

During some time early in summer 2010 I started to feel like I was going to die. Maybe not the next day. Maybe not the next month. But maybe in some of the next years, not too far away, I felt I would become an ex-parrot not too far in the future. And if my illness wouldn't put me down, I would have done so myself.

Health problems of mine, that weren't good since my youth, took a turn for the worse. My energy level took a steady dive. Caffeine was the only thing that kept me going through day after day, and only barely. I needed two hours to get out of bed.

Then new symptoms started to appear.

First there was a "pressurized feeling" in the back, whenever I got stressed. This pressure was on both sides, localized, not broad, where I would suspect the kidneys are. After a month or two, this "kidney pressure" during stress" turned into "kidney pain" during stress. Very focal pain. Not too strong, but very nasty pain. Might have been the adrenals.

Now I know that I have primary adrenal insufficiency, the real kind, confirmed through two salvia tests and an ACTH stimulation test – not too "strong", mind you, my luck I can't even get a full blown primary adrenal insufficiency. So the "kidney pain" back then might have been adrenal pain. And adrenal insufficiency explains some of my symptoms, but not all.

Anyway, back to summer 2010. The adrenal pain wasn't the only new thing. Strange feelings on the skin. Very unpleasant skin sensations, that made it difficult to touch e.g. a trackpad.

I initially took a "psychosomatic" view of my ailments. I am not motivated to get out of bed in the morning. I am stressing myself too much. The pain is psychosomatic response to pain. All that bullshit.

I really tried hard to battle my problems from an idealistic position. Aided by the people I were with at that time, who had an explicit idealistic position when it came to health.

As if pain wasn't a real warning sign for bodily problems, as if it could be "willed away".

Anyhow, while I managed to manage some details, most of my symptoms got worse. Steadily. Downwards. Something else had to be done.

Little did I know about humans and illnesses back then. But I knew a little bit about type 1 Diabetes, have heard of type 2 Diabetes, of obesity, of "metabolic syndrome". So I looked into nutrition. Stumbled across Wolfgang Lutz and his book "Life Without Bread" ("Leben Ohne Brot"), and stumbled across Robert Atkins and his diet. Both are about reducing carbs, and as the regulation of carbs/insulin is broken in Diabetes, reducing carbs might be a good idea, I thought. (Today I know that an optimal diet is probably closer to an Paleo diet, and that carbs are not bad in general, but rather some foods containing carbs – like grains and dairy – are probably to blame for health problems)

As I felt I was going to die some time sooner that later anyway, I ignored all the well-meaning warnings about these diets ("You need grains! Blah blah!") and gave it a shot.

And what can I say, my health improve. Improved fast. Improved markedly. Symptoms waned and faded away. I got energy in the morning, to get out of bed soon after waking up. I started to feel like a human being for the first time in my life, not a sack of flesh dragging myself through life.

One of the predictions Atkins made was that his diet would be ketogenic, and that is what this ketogenic property that helped the body heal. And sure enough, when I meassured the so called ketones with ketosticks, sure enough the diet was ketogenic.

But the ketogenic property of the diet faded away, as Atkins predicted – the ketosticks confirmed it. And with the ketones faded the energy.

The good thing that with a Paleo diet a considerable share of the health problems stayed away for good – but my energy levels were in the gutter again.

So for some time I had the idea that I need to get back into a ketogenic state to get my energy back. It took me some time until I tried an shot at an proper ketogenic diet. Ketogenic diets are a bit demanding, as you need to reduce carbs and increase fat consumption, increase fat consumption massively.

So I tried a ketogenic diet, to get back to an ketogenic state. And lo and behold, with some considerable effort I was able to get my ketones up. Measurable up.

Unfortunately, the positive health effects, that I had the first time my ketones were up, that positive  health effects did not return with the ketones.

So I have to report a negative result with regards an effect of an ketogenic diet to my illness (whatever that illness is).

As a note, I have heard that the ketogenic diet might be useful for other illness (like epilepsy and migraines). Good information on ketogenic diet can be found at the Perfect Health Diet blog – don't expect too much though: Your milage may vary; A Paleo diet helped me to some considerable degree, but a ketogenic diet did not improve above that.

What I can recommend is to experiment with an Paleo diet, and to be careful not to attribute health problems to one certain product too fast ("my X is caused by Y!").

As an example: To test the influence of e.g. dairy on your health, you need to get rid of all dairy for at least a month (even milk-chocolate!), then reintroduce dairy (make a "challenge"), see the effects (if any), then go dairy free again for at least two weeks, to repeat the challenge once more. Only if after two or three challenges you see consistent results, then you can say that the problems are caused by dairy. You could (and should!) repeat this with other foods, like grains (bread, cereal), or with potatoes.

Tuesday, September 4, 2012

Raw milk, acne and blood sugar – An update

As I wrote before, my acne is caused by milk. While I sometimes get very very very small furuncles (which i haven't been able to track down to a cause yet), I just need to east a bit of dairy to get several nasty furuncles and sometimes even nasty pimples. No doubt, milk caused my acne, which I can say with certainty after being dairy-free for quite some time now.

Now I wanted to see if raw dairy (from non-pasteurized milk) makes a difference, as I read something to that effect. I got some really nice raw-milk "Bergkäse" cheese, and ate a nice piece of it.

And what can I say about raw-milk dairy, after a sample size of 1?

The good: 
No acne. None whatsoever. And the Bergkäse was really nice.

The bad and ugly:
I ate the cheese at 10 in the morning and about half an hour later I got a rather low blood sugar: All the symptoms like "that jittery feeling", and the confirmation by several measurements of blood sugar (blood glucose) during the day. Eating some glucose, and then some more didn't help much. And then some potatoes, and then some more. I was jittery to some degree all day. And had (slighter) problems with blood sugar for some days.


I need to try this experiment again, in some weeks, to see if this is not some random fluke.

At least for now, and for me, it seems that (pasteurized) milk is able to provoke an immune reaction (in the form of acne) in my body – this could provide an plausible mechanism for some autoimmune conditions.

And it seems possible (for now) that milk fucks up the insulin/blood sugar regulation of my body – something I need to confirm† or rule out‡. Next time

Update: Just one short update, a second try with raw-milk cheese, and I did not get any noticeable bad health results. Let's see.


† Confirmation that milk fucks up insulin/glucose regulation would be really really cool, as it would provide an mechanism for some of the diseases we see – say: obesity, "metabolic syndrome", T1DM and T2DM (type 1/2 diabetes mellitus)

‡ Ruling out negative health effects (for me) of raw milk would be really really cool, as I could eat cheese again, in the form of raw milk cheese.


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