As you may have seen in my Diet and Obesity article, diet does play a role. Based on what I know about the pathogenesis of chronic disease, I don’t think it’s the primary role. Take a look at the Pathways study alluded to in that article. That intervention was first-rate. Why did it fail? It is my opinion that a dysregulated vitamin D metabolism is to blame, a variable not addressed by the Pathways study.

Best,
Amy

I think Ken (above) brings up an important point when he says

‘…Even if she cleansed her body of the “bad” bacteria, wouldn’t she just become re-infected again by exposure to my daughter, as well as her friends and family who carry the “bad” bacteria?

In fact, doesn’t this point out a flaw in the MP treatment? Isn’t it only half of the answer? …’

Don’t you suppose that our modern diet contributes to L-form bacteria being able to take up residence in our bodies in the first place? Do you think that eating excessive carbohydrates (or additives, or trans fats, or other damaged food) alters our body chemistry in a way that provides a welcome environment to th1?

Have any studies been done regarding diet and eradication of L-form bacteria?

Maria

I should have been more specific when I mentioned the possibility of putting your nanny on the MP. Essentially, once people are taking Benicar and a reasonable dose of the MP antibiotics, the chronic bacteria they harbor are killed before they are able leave the body and are spread to other people.

For example, my boyfriend and I have been together for three years. We are both on the MP and both have very different symptoms. But we are not worried about trading bacteria because we are both on the MP and thus our bacteria are too weak to spread. At least neither of us is showing either of the other’s symptoms.

Your nanny is heavy, and the MP takes a long time to complete. I also expect that with her weight problems come other Th1 related problems, as is the case with most of our other subjects. So she would probably be on the MP for a good 3-4 years during which time I don’t think she’d pass your daughter much of anything.

When it comes to the period after she stops the MP I recommend reading the following short piece about what state people are in when they stop the treatment:

http://bacteriality.com/2008/02/23/misconceptions/#13

The MP does two things – it kills the bacteria causing inflammatory disease and it also strengthens the innate immune response. So a person who finishes the treatment has excellent immune function. So if your nanny did complete the MP she would pick up chronic pathogens again at a very slow rate. And since all of the population harbors the Th1 pathogens to a certain exten, she’d certainly be the person you would most want around your daughter as any other older women would have her own share of bacteria.

MP patients who have stopped the treatment generally do “touch ups” every few years (as described in the piece) which keep their bacterial load very low.

As for supplementing with “good” bacteria, I’m skeptical of the benefits. Usually the body works best when (after being rid of chronic bacteria) if is allowed to return to homeostasis on it’s own. Even “good” bacteria place an extra load on the innate immune system and may be able to trade DNA with less innocuous pathogens.

It’s sort of like some of the instances in which a certain animal has been introduced to a habitat in order to kill a pest and the second animal ends up causing more problems than the first. That may not end up being the case with gut bacteria, but the gut is definitely an unknown “habitat” at this point and we don’t want to artificially skew it’s composition too much, at least for now.

Best,

Amy

I’m not sure if using the Marshall Protocal on the nanny would do any good. Even if she cleansed her body of the “bad” bacteria, wouldn’t she just become re-infected again by exposure to my daughter, as well as her friends and family who carry the “bad” bacteria?

In fact, doesn’t this point out a flaw in the MP treatment? Isn’t it only half of the answer. In order to prevent re-infection by the “bad” bacteria wouldn’t a person have to innoculate themselves with “good” (i.e. thin) bacteria to prevent re-infection?

It would seem unlikely that a random innoculation with “good” bacteria would happen, since the steady spread of the “bad” bacteria in society suggests that it is better at defending its territory than most “good” bacteria. In fact, the spread of the “bad” bacteria suggests that even if a person was innoculated with “good” bacteria it might only be a matter of time until they were reinfected with the “bad” bacteria. Perhaps this is a partial explanation for why Kathy (who takes antibiotics for sinus infections) continues to have weight problems even after taking mega doses of antibiotics.

Has any research been done into locating a super-good bacteria that could defend its territory against the infection of “bad” bacteria? Perhaps taking cultures from thin people who are surrounded by overweight people but resist gaining weight themselves might locate a naturally occurring strain of super-good bacteria. This strain could then be used to innoculate people who underwent the MP treatment.

Has anyone looked into these issues?

Answering this question makes me feel somewhat uncomfortable. I know what I say could affect whether someone gets to keep her job, and that is a responsibility I would rather not have.

That said, in my opinion, the answer is yes.

Bacteria are passed by close contact with others. One doesn’t even need to share utensils. Humans are especially vulnerable during their first weeks of life when the innate immune system has not been fully formed. (Did your family’s nanny work for you then?) For more on this topic, have a look at my Babies and bacteria article.

Some might say that obesity isn’t contagious, but how else would you explain this prediction, which says that all Americans will be overweight by 2040? To suggest that the recent and future epidemic in obesity is merely learned behavior is a cop out. We’ve seen multi-year large-scale interventions designed to curb obesity fail.

The genetic explanation doesn’t hold much more promise: it’s simply impossible for a genetic model to account for such a rapid escalation in rates of obesity.

To return to your original question, the only suggestion I might offer is that you (delicately) encourage your nanny to do the MP.

Best,
Amy

Ken

Oh man…I know what you are talking about! Before the MP my cravings for food and carbohydrates in particular were off the roof. I mean, it was out of control. All I ate were carbs – muffins, “energy” bars, bread – I simply could not feel satiated unless I ate some huge serving of carbohydrates and then I’d literally be hungry again half an hour later. At night I’d binge eat on sweets – it was nuts.

Now my carb cravings are completely gone and get this – I am actually able to eat a no/low carb diet. I never thought that possible, and when I decided to try the diet I was so sure that I would fail. But I managed one day without carbs and amazingly didn’t even miss them, the next day I was fine…I haven’t eaten bread for months now and don’t even think about it. What a different world.

Anyway, the point of that whole description is that yes, I believe the carb cravings are related to the presence of bacteria and the inflammatory disease process. Because when my inflammation was at its worst so were my cravings, and now that my inflammation is significantly less so are the cravings.

There are several reasons I came up for why I used to have insane carb cravings. All are theoretical, but I’ll share them.

1. When my disease was at it’s worst just dealing with the high load of pathogens put my body under so much stress. My body was fighting a war every day just to stay alive with so many bacteria and other pathogens wearing it down. This put me under tremendous stress. The most immediate source of energy to keep my body going while it was dealing with this stress was carbs – which are broken down into glucose that the body can use quickly. Hence the cravings.

2. Many L-form bacteria use carbohydrates as a source of energy. Knowing know that most bacteria use glucose as a source of energy I can imagine that all my pathogens were “crying out” to be fed – inducing the cravings.

3. Researchers at McGill University in Canada have shown that the Vitamin D Receptor transcribes several key genes that regulate insulin and allow for the formation of the insulin receptors. When 25-D and ligands created by all the bacteria I was carrying blocked the VDR, the production of these insulin-related genes was blocked as well, causing havoc on my body’s ability to regulate blood sugar. I’m sure I had unusual fluctuations in blood sugar that could have contributed to the cravings.

Those are my best explanations. Maybe it was a combination of all three or maybe another process was going on that I am not aware of. All I know is that the cravings are gone, so lowering inflammation and killing L-form bacteria are a way out of the craving situation.

Best,

Amy

I’ve been following the MP for a few years now due to Sarcoidosis and I’ve experienced episodes where cravings and hunger seemed to be exacerbated. I’m certain that I have nervous system involvement and inflammation – maybe that’s the key? Or could it be dis-regulated blood sugar or other hormone signals that arise from inflammation?

Have you found any research into what drive’s our hunger for food and how a dis-regulated metabolism could upset it?

To my knowledge nobody has tried using the Marshall Protocol to treat MRSA – but that doesn’t mean that the treatment doesn’t have a high chance of killing the resistant staph species that cause the disease. That’s because the MP has been carefully designed to target persistent and difficult to kill bacteria that other antibiotic treatments cannot touch – and it does this very effectively.

I have talked with Dr. Marshall personally about MRSA and the Marshall Protocol since my twin sister’s boyfriend has MRSA. In a few months he will be starting the MP to treat his infection because Dr. Marshall believes that the it is highly likely that the MP will work for him.

I encourage you to do the same and try using the Marshall Protocol to treat your MRSA, as it is definitely the treatment with the greatest hope of working against resistant staph. Your other alternatives are not very good, as the high dose antibiotics used to treat MRSA kill some forms of staph but leave staph L-forms behind and alive, which means people are likely to relapse at a later date. Read more about L-form bacteria here.

http://bacteriality.com/2007/08/15/l-forms/

I’m not saying that high does antibiotics shouldn’t be used at some points, only that the MP will kill any staph L-form which is necessary if the infection is to clear completely.

I recommend that you post further about this issue at the following website – http://www.curemyth1.org (Th1 refers to disease caused by treatment resistant bacteria, hence the name Cure My Th1)

The patient advocates on that site will answer your questions about MRSA and the MP in greater depth. There is no charge for their advice and no charge to use the Marshall Protocol as the study sites are run by a non-profit organization.

Good luck!

Amy