Retraction and clarification.

In a previous post I recommended several therapies for Crohn’s and as I research more I must retract / re-examine some of this.

I no longer believe DMSO to be safe for human use. It’s been shown to cause apoptosis (cell death) of retinal cells in mice. You can take this at your own discretion but I will no longer advocate its use due to this finding.

DHEA may not be safe to use without being overseen by a doctor specializing in hormone therapies. Due to the complex nature of hormones in our bodies, it’s possible for DHEA supplementation to destabilize our natural hormones resulting in hair loss and opposite-gender traits (facial hair in women, gynocomastia or male breast tissue).

Think Volume for Size

Sometimes people in the gym get so caught up in trying to put more weight on the bar they forget about one of the longest known strategies to pack on the hypertrophy, and that’s high volume training.

The problem with heavy weights is your muscles will reach absolute failure before they can receive the same amount of stimulation they could from a lower weight, high volume routine.

While these heavy weights are ideal for training the central nervous system to adapt to heavier loads and activate  more muscle fibers in a single repetition, it may not be as good for the completeness of stimulation that leads to muscular growth and hypertrophy.

Let’s say you’re an average, healthy, gym-going male and your 5 rep barbell curl max is about 80 lb.s, that’s with minimal back sway, strict form.

You can probably do 3 sets of your 5 rep max before your arms are pretty well done lifting that weight for the day.

But if you lowered your weight to about 65, you could lift it maybe 12 times.

What I want you to do is find the weight you could lift exactly 12 times and instead I want you to do 5 reps with it, then rest for 30 seconds, and repeat 5 times.

So for our theoretical lifter here:

65 lb.s x5

30 second rest


30 second rest


30 second rest

x 5

Now they’re just lifted 65 lb.s 25 times over the course of a few minutes which is a cumulative 1625 lb.s of load.

Whereas if they lifted their 5rm of 80 lb.s 15 times in the same time span you’d be looking at 1200 lb.s of total load.

Already you can see where a lower weight can start to add up.

Now once you’re finished with your FINAL set of five, I want you to immediately grab a bar that’s 10 lb.s lighter, or if you’re using dumbbells, 5 lb.s lighter on each side. Do 5 more reps. Drop the weight another 5 lbs and repeat.

If you absolutely have to take a break, do so, but continue this until you can’t even lift the 5 lb dumbbells then call your biceps done for the day.

Micronutrients, the importance of testing for deficiencies.

Our dietary makeup breaks down from our caloric total to the macro nutrients that made it, which is fats, proteins and carbohydrates.

Within these we find the micro nutrients, or more commonly known as vitamins and minerals. The quality of food you buy will effect the quality and quantity of your micro nutrient content. Depending on your dietary variety, geographic location, and various environmental and lifestyle choices, it’s likely many of us will have deficiencies in one or more micro nutrient, and it’s important to get a clinical diagnosis before trying to address these issues.

Minerals, especially, can be dangerous in excessive doses as well as in depleted quantities. They also exist in antagonistic relations with one another. For example, Zinc and Copper compete, and taking one may decrease the amount of the other.

This is why it’s important to know if you’re deficient in one or both before taking either supplement. Taking zinc with a copper deficiency could deplete your copper to dangerous levels.

Some micro nutrients come in a variety of sources, and some are safer to take in high doses than others. Vitamin A sourced from plant-bases like beta-carotenoids are safer than those from preformed meat-based sources. It’s very difficult to take too much from a plant-based source.

Likewise the reaction your body has, and the bio availability of sources differs. The oxide form of many minerals found in cheap drug store multivitamins will not be as easy to absorb as citrate or other forms acidic forms. This is why the calcium found in milk may not be as useful as calcium citrate in a supplement form.

Contact your doctor for blood and urine testing if you believe you are deficient in one or more micro nutrients.

A trick to combating fat and obesity that works…

I may have to retract things I have said in the past. I can’t recall if I’ve ever explicitly stated it in this blog, but for a long time I’ve been a follower of the idea of “If It Fits Your Macos” (IIFYM) dieting.
IIFYM is often summed up in an over simplified manner as ever calorie from every carbohydrate source has the same value to your bodyweight no matter if it’s from rice, grains, sugar, poptarts or icecream. 500 calories of carbs from ice cream has the same weight gain potential to your body as 500 calories of whole-wheat bread.

Now there’s evidence that not only is this untrue in the immediate short term digestion, but over time you can alter the way your body responds to calories and gains weight, even combat obesity. This suggests that obesity might not be solely the result of over eating.

Mounting evidence suggests that the microbiome of the intestines, that is the bacteria in our large intestine that help us digest our food, are responsible for how our bodies respond to intake of certain foods. We have four primary families of bacteria but the most important for our purposes are the Firmicutes and Bacteroidetes.

In those with obesity we see a decrease in Bacteroidetes and an overgrowth of Firmicutes. This may be something they were born with, brought on by environmental factors, or it could be caused by long-term bad diet.

Recent evidence suggests that growth and death of different gut bacteria is in response to our food intake. Firmicutes thrives in a diet high in fat and sugar. Bacteroidetes however feeds on complex carbohydrates, starches and plant matter as well as our intestinal mucins when in a state of starvation. This is a good thing for those looking to control their weight which I’ll explain shortly.

So how can I apply this to weight loss?

There’s a few things you can do to help rebalance your gut bacteria in favor of healthy Bacteroidetes populations.

Eat more starchy fruits and vegetables

This includes potatoes, plantains, green bananas, to name a few. Overall though, there’s not really a wrong answer here. Fruits and vegetables are healthy sources of complex carbs, vitamins and minerals and the more of these you eat the less junk food you’ll have room for.


Bacteroidetes is more resilient to starvation that its counterpart. In a fast bacteroidetes can consume intestinal mucins to stay alive where other bacteria will gradually starve out. I’m not advocating long term starvation diets or water fasts, but healthy intermittent fast for 16 hours a day, or fasts with only green drinks or restricted zero-carb dieting for large portions of the day, even up to 72 hours could potentially effect the balance of bacteria. Remember though, our intestinal bacteria is very resilient and changing it is a LONG TERM plan, so any diet you choose needs to be sustainable. You can’t hope to crash diet your bacteria into the way you want. As soon as you go back to eating sugary, fatty food you’ll go back to the way things were.

Eat LESS junk food

This shouldn’t really need explaining. Junk food feeds the bad bacteria, it’s high in empty calories, low in satiation, and it’s bad for your long term health. Simply reducing your daily intake may not be enough for those with advanced weight gain problems. You need to commit to a lifestyle change for the long term if you want to reap the benefits.


The other side of the coin. What if MAP is innocent?

In a previous post I’ve mentioned the theory of MAP bacteria being implicated in the pathogenesis of Crohn’s disease.

There’s evidence suggesting a connection, and treatment of Crohn’s with antibiotics has shown positive results, however this doesn’t give us a definitive answer on the involvement of MAP as a causative factor in Crohn’s disease.

In my last couple of blog posts I discussed how bad diet mixed with dysbiosis of the gut and loss of healthy gut flora can leave vacancies in the ecosystem of the intestines that can be filled by overpopulation of harmful bacteria. These include bacteria like klebsiella, AIEC and MAP just to name a few.

Fingers have been pointed at each of these bacteria in turn as the ‘causative’ factor in Crohn’s. After all, it makes sense. They’re in the intestinal wall, they’re harmful, they’ve been found in a large number of patients and they tend to manifest in ways that are present in Crohn’s symptoms.

I think the problem here comes back to the chicken and the egg argument. It’s possible these bacteria are causing  many of the symptoms associated with Crohn’s, but they are not the cause of Crohn’s itself. You can cure the patient of the bacteria, but they will still have Crohn’s, and unless you can find a way to rebuild a healthy gut ecosystem, the bacteria could come back, and become resistant to the antibiotics you used to treat them.

I’d like to link to a very interesting discussion with a Crohn’s researcher on the Crohn’s Disease forum with some great supporting evidence to this end:

Not like saccharin and sucralose, MAP as the possible cause of Crohn’s disease had been suspected for about a century, with extensive studies by some researchers, especially in the last several decades. Despite that, the results remains highly controversial, largely because the conflicting “facts” in almost every aspects. To my knowledge, there is also a big discrepancy between the incidence of IBD and contamination of MAP in some countries. For instance, Sweden had been one of the countries with the highest incidence of IBD, including both CD and ulcerative colitis (UC), but MAP contamination had been extremely low (see Sternberg Lewerin S et al. Control of paratuberculosis in Sweden. Proceedings of the 9th International Colloquium on Paratuberculosis 2007, p. 319-323.…ories/pdfs/274). Back to 1952, MAP had been included in the Swedish Epizootic Act (SFS 1999:657). According to this legislation any suspicion of MAP is notifiable for animal owners, veterinarians or other professionals with animal contact, regardless of the species of the animal. Moreover, it required the Swedish Board of Agriculture must investigate all suspect cases and take all necessary means to eradicate and prevent the spread of the infection, if confirmed. As the result, although there were a few sporadic cases of MAP infection in cattle since 1993, all the cases were directly or indirectly linked to the imported animals, with all cases being beef herds, but none in dairy herds. The negative finding of domestically originated MAP in the more than 1.5 million of cattle and about half a million of sheep all over the country suggested the extremely low, if not zero, MAP contamination in Sweden, despite the very high incidence of CD and UC seen in many cities in Sweden like Stockholm, Uppsala, Orebro, Malmo, and Gothenburg.

In addition, there were also many conflict results regarding other aspects on the suspected link between MAP and IBD. Although some studies (like the one in Forest Virginia) suspected that contamination of MAP in the pasteurized milk or the water supply may cause CD in human, other studies failed to show any increased risk for dairy farmers with a more direct and certain contact with MAP through the infected animals (Jones PH, et al. Crohn’s disease in people exposed to clinical cases of bovine paratuberculosis. Epidemiol Infect 2006;134:49-56). Although study indeed found MAP in the lymph nodes of feral cats on the contaminated farm, they did not had the signs of IBD (Palmer MV et al. Isolation of Mycobacterium avium subsp paratuberculosis (Map) from feral cats on a dairy farm with Map-infected cattle. J Wildl 2005;41:629-35).

At beginning people were suspected a similar origin for both Johne’s disease in cattle and CD in humans as they both showed the obstructive damage near the end of the ileum. However, as shown in some of the recent studies, there was a shift of CD from the small intestine to large intestine over time and the involvement of only large intestine has become the main form for CD (the Crohn’s colitis). I suspected that IBD now would be more mimic the commonly seen IBD in pet dogs and cats rather than the Johne’s disease in cattle (Qin X. What is human inflammatory bowel disease (IBD) more like: Johne’s disease in cattle or IBD in dogs and cats? Inflamm Bowel Dis. 2008 Jan;14(1):138). There were also many other fundamental differences between Johne’s disease and CD. For instance, large amounts of MAP can be found in the mucosa or feces of cattle with Johne’s disease, which can be transmitted to healthy herds; in contrast, the bacteria are hardly seen in the tissues and feces of patients with CD, and IBD in general is regarded as noncontiguous. Although studies showed higher rates of existence of MAP in gut tissue of CD patients by the high sensitive methods such as the PCR detection of the IS900 DNA segments, there are also increase in other bacteria such as Helicobacter spp., Listeria monocytogenes and Escherichia coli, suggesting this could be just reflected the weakening of gut barrier and increased gut permeability (Tiveljung A, et al. Presence of eubacteria in biopsies from Crohn’s disease inflammatory lesions as determined by 16S rRNA gene-based PCR. J Med Microbiol 1999;48:263-8). Finding of viable MAP in patients with CD would be important evidence for the possible link. However, the more rigorous test organized by NIH failed to repeat and confirm these findings (Van Kruiningen HJ. Where are the weapons of mass destruction – the Mycobacterium paratuberculosis in Crohn’s disease? J Crohns Colitis 2011;5:638-44). Therefore, it would be no surprising that there are many deep believers on both sides. Both sides think they hold enough scientific evidences. However, one thing would be true: one side must be wrong, along with the many “solid scientific facts”.

In summary:

-Sweden, a country with strict control of Johne’s in animal population has disproportionately high levels of IBD

-Germany, a country with high incidences of Johne’s in animal population doesn’t show a proportionately high level of IBD cases

-MAP is notoriously hard to culture from human IBD patients, but easily tested for in livestock

-Farmers who are directly exposed to livestock do not show an increased IBD rate of occurrence

So we know that MAP is more prevalent in the bowel of Crohn’s patients than the general population. We also know that treatment targeting MAP with antibiotics often yields positive results. Doesn’t this contradict itself?

Not necessarily!

The dysbiosis associated with Crohn’s disease could simply be paving the way for MAP which was already present and controlled in healthy individuals to grow freely. Higher levels of MAP could simply be a marker of increased intestinal dysbiosis caused either other factors of Crohn’s. The presence of these bacteria could be a good marker of the deterioration of overall intestinal mucosal and bacterial health, and treating them could lead to improvement of symptoms, but it remains to be proven if any particular bacteria can be implicated as the causative factor of the disease.

It may also, then, be possible to protect yourself from worsening of the disease by altering your diet to combat dysbiosis and growth of these invasive bacteria. By building up the intestinal mucosa one can prevent their ability to cross into the intestinal wall or blood.

Eat away those food intolerances.

I recently made a post on gut bacteria as it relates to food intolerance. I shared the literature I’d found with some members on Crohn’s Forum and was asked what I would recommend to a patient if I was to suggest a therapy targeted at repopulating gut bacteria?

I’m going to link back to this study which is where I get much of my information.

This is highly theoretical, and my knowledge is not perfectly well rounded on this topic, and I will admit that as I go! If you can expand on any of the topics I discuss here, or find issues, I implore you to contact me at my goal is to get the population THINKING about these topics, not to become a first rate source of primary medical advice.

My digging into this topic is still fairly new to me, but given what I’ve already read I have formulated an early dietary strategy which I intend to apply. Here’s how my post was detailed:

Therapeutic Diet for Managing and Improving IBD Related Symptoms and Food Intolerance

I’m still building on it with self experimentation. The problem would be that I would need to create a different diet for each patient based on their digestive capabilities.

It seems evident that our food intolerances are based on both the level of dysbiosis and the specific imbalances. For example the reason that some patients can have lactose but others cannot is likely due to either insufficient bacteria of the kind that consume it in the lower GI tract, or overgrowth of harmful bacteria that consume it in the upper GI tract. I think we need testing on the specific bacteria loads of healthy individuals vs. ones with specific food intolerances to see what those differences are so we can better understand what needs to be taken out or put back in.

Mine are VERY limited right now, IDEALLY I would include a higher balance of prebiotic foods in my diet but I cannot tolerate the ones I want to, while many other Crohn’s patients can.

I can tell you a rough idea of an approach I would use based on the chart I found describing bacterial growth as relates to diet.

Summary of diet-induced dysbiosis

Diet Bacteria Altered Effect on Bacteria References
Bifidobacteria spp. Decreased (absent) [45]
High-fat and high-sugar
Clostridium innocuum, Catenibacterium mitsuokai and Enterococcus spp. Increased [18]
Bacteroides spp. Decreased [18]

Bacteroidetes Increased [49]

Clostridium coccoides, Lactobacillus spp. and Bifidobacteria spp. Decreased (growth prevented) [48]

Complex carbohydrates
Mycobacterium avium subspecies paratuberculosis and Enterobacteriaceae Decreased [49]
B. longum subspecies longum, B.breve and B. thetaiotaomicron Increased [53]
Refined sugars
C. difficile and C. perfringens Increased [54,55]

E. coli Decreased [56]
High n-6 PUFA from safflower oil
Bacteroidetes Decreased [59,60]
Firmicutes, Actinobacteria and Proteobacteria Increased [59,60]
δ-Proteobacteria Increased [61]
Animal milk fat
δ-Proteobacteria Increased [62]

Stage 1 diet
My first step would be to test for SIBO and the prevalance of harmful / invasive species like MAP, C. Diff, and Klebsiella because if those are a problem it limits your dietary options further. Simple sugars would DEFINITELY be off the table. Klebsiella also limits your use of standard prebiotics like RS, FOS and inulin because it’s capable of breaking the complex molecular bonds that divides them from simple sugars.

So my first treatment for those with SIBO would be one of a few things. The safe approach would be a mixture of complete carb restriction and intermittent fasting, which risks further imbalancing the gut flora in favor of bacteroidetes, but unfortunately the only other choice is powerful antibiotics which will have the same result, but with a possibly more dramatic die-off of good bacteria. It might require several antibiotics taken at the same time with bad side effects to kill off these bacteria without dietary changes.

I would restrict the diet initially to meats, broths and tolerable oils focused on safflower and coconut oil, basically a fully ketogenic diet until they see a decrease in invasive bacteria. Due to extreme restriction of diet I would also put them on a multi vitamin. I would say this approach should be completely safe, supplementing with probiotics would be optional but not necessarily effective due to the chances you’d simply be starving them out anyway. Caprylic acid supplementation is also an option that I would consider safe but not sure if it’s effective. You’d already be getting some in coconut oil.

Grey area

For a more pseudo-science approach, I would say it’s -possible- but not yet tested to the point of recommendation to supplement with eugenol and carvacrol containing oils like thyme, oregano and cloves, black wallnut,wormwood, cinnamon, basil and bay leaf which have been shown to kill harmful bacteria while feeding Firmicutes strains. Until I can find further evidence on the safety and effectiveness of this therapy I would file it under a ‘maybe.’ I would like to further look into if taking them with an enteric coating to deliver them as food to the large intestines + fight off harmful bacteria there would be effective / optimal. So far search results on the topic have been no help.

Stage 2 diet
After the invasive bacteria is under control I would introduce complex carbs starting with low dose resistant starches like psyllium husks, potato starch (if tolerable), green bananas or plantains along with supplementation of FOS and inulin since foods containing it will likely be hard to digest for a patient with advanced dysbiosis due to high fiber content.

Initially they would likely experience flatulence, bloating and possibly diarrhea or constipation, so moderation and gradual increase based on personal comfort level would be necessary. Continued testing would be important to see that levels of harmful bacteria remain low and aren’t feeding on the prebiotics.

Grey area
As you begin to introduce prebiotics, over the next week or so I’d say start introducing probiotics targeted at bringing up the shortcomings in their bowel diversity. Unfortunately it doesn’t seem like there are capsules or anything for Clostridia, but it’s likely Bifido bacteria would be the first choice which is a protective bacteria many Crohn’s patients are deficient in.

This is another area I need more research in. When do you introduce probioitics / prebiotics? If you introduce the prebiotics first with nothing to feed you could be feeding the already over represented bacteroidetes. If you introduce probiotics without prebiotics as food for them they may starve. Will both at the same time simply cause too much gastric upset (flatulence, diarrhea etc.) for the comfort of the patient? How long will it take to subside? This is another area I need to find hard information on.

I would look really hard at supplementing L. acidophilus in those with lactose inolerance and possibly colostrum supplementation which acts as another natural prebiotic. I need further research to confirm effectiveness of both.

Stage 3 diet
Ideally the patient’s food tolerances should continue to improve until they are able to move onto a diet rich in raw fruits and vegetables from which they can get their vitamins and prebiotics, along with meats, animal fats and healthy oils like safflower, and extra virgin coconut and olive oil. This would be the end goal for long term maintenance of healthy gut bacteria.

For those with complications of Crohn’s like having had resections it could complicate the effectiveness because bacterial populations are regional to the intestines and I have no evidence of whether those populations can migrate and what effect that has on the ecosystem of the gut.

Grey area
I would look at raw, organic honey and royal jelly as a prebiotic for those in the advanced dietary stages with no signs of SIBO. I think regular testing for SIBO until dietary effectiveness is established would be best. I have reservations about honey though because some say harmful bacteria cannot digest it due to its chemical structure, while others say it can. I’d really like a confirmation on this but it doesn’t seem that many find it scientifically relevant.

Long term maintenance, comparison with obesity etc.
Over the long term, it looks like a diet rich in complex carbs and fats with moderate protein will lead to the ideal balance that we’re looking for. We basically want to be eating what obese people eat – because they have an overgrowth of Firmicutes where we have the opposite. We’re unfortunately prevented from the large intake of simple sugars typically associated with obesity because it promotes SIBO.

So what do we have to learn from this? Well unfortunately both the bacteria that we want, and the one we want to reduce depend on carbohydrates to an extent. Firmicutes seems to love fat and sugar – but bad bacteria also love sugar, so sugar binge eating is not an option to us!

Firmicutes is much less resilient to starvation than Bacteroidetes. If an obese person combined fasting with increase of resistant starches, they’d see a reduction in firmicutes and an increase of bacteroidetes.

Fasting and how it relates to this
For this reason I support the continual small meals through the day approach for Crohn’s. In the past I’ve spoken in favor of fasting for Crohn’s so let me clarify why I believe it’s not the OPTIMAL approach, and will advise against it except as a SIBO therapy until I can further investigate its effects on Bacteroidetes and intestinal flora.

During a fast we see a loss of firmicutes as well as harmful bacteria, an increase of gut-based serotonin production, and increased catecholamine production, increased cortisol production. All this is beneficial to Crohn’s healing EXCEPT the loss of firmicutes.

We also see the Bacteroidetes begins to consume intestinal mucins to avoid starvation, as a biproduct is creates butyric acid which promotes mucosal healing. So we see healing of the mucosa, balancing of the neurotransmitters, and bowel rest, great stuff really.

But we also see death of Firmicutes which leads to furthering of food intolerance. I don’t have the resources to prove if one can maintain / grow their firmicutes population during the 8 hour feeding window of an Intermittent Fasting diet, so until I sure, I deem fasting to be counter-productive to the goals of expanding dietary food tolerance.

Dairy and MAP
I’d like to make a fleeting mention of dairy. I’m starting to believe that MAP bacteria is not the primary cause of Crohn’s, and that it’s simply a result of the dysbiosis we see, and a marker of the loss of protective bacteria and overgrowth of harmful bacteria. It’s likely that the high prevalence in Crohn’s patients is a sign of overall bad gut health, and it’s possible that it DOES cause symptoms, however we also find it in healthy, asymptomatic individuals. I think in advanced dietary recovery with L acidophilus supplementation I would consider dairy to be SAFE and that the MAP should be manageable if you can restore a healthy balance of gut bacteria to protect you from it. I think monitoring of symptoms and levels of MAP in a patient in the advanced stages of the recovery diet would be very interesting to give us a better perspective on the role of dairy consumption and MAP growth.

My opinion on dairy is, perhaps, biased because I’ve NEVER seen correlation between dairy and my symptoms except when consuming it at ABSURD levels (1 gallon whole milk a day). The one time I experienced problems with dairy, I supplemented Kefir for a couple weeks and the problems subsided.

I’d like to post-edit this section to include a link to this article

With more information on gut dysbiosis as a cause of lactose intolerance. 

Thoughts on another promising dietary supplement:

I just found this, I read about it before but forgot to mention it because there’s just so much stuff I’ve read lately I forget some things.
Polydextrose seems extremely promising in its ability to rebalance gut bacteria.

[QUOTE] Short-chain fatty acid production—notably that of butyrate, isobutyrate, and acetate—increased with polydextrose ingestion. There were substantial changes in fecal anaerobes after polydextrose intake. Bacteroides species (B. fragilis, B. vulgatus, and B. intermedius) decreased, whereas Lactobacillus and Bifidobacterium species increased. [/QUOTE]

[QUOTE]Conclusion: Polydextrose ingestion had significant dietary fiber–like effects with no laxative problems.[/QUOTE]

This is EXACTLY what we want.

I will definitely be looking into polydextrose, possible adverse effects, and seeing if I want to try it myself in the near future.

Gut bacteria linked to IBD, Crohn’s & Obesity.

I’d first off like to link to this blog which was part of an important trigger in sending me down this path of research, because until I found it I was very much in the dark about the human gut microbiome and I believed it was just too poorly understood to warrant further internet research.

It is from this blog I get much of my info, or was directed onward to sources that have it. It is some heavy reading, so I decided to condense some of the important take-aways for the more casual reader.

The human digestion is populated by a large variety of gut bacteria, these bacteria fall into families that sub-categorize them. Among these families two of the largest and most important are the bacteroidetes and the firmicutes. These two exist in what is almost a direct competition of one another. They feed on similar food resources, however create two different environments in the gut, and thus have different effects on the body itself.

Firmicutes, including the clostridia strains, aids in many functions of the gut including production of protective butyric acid and is involved in prevention of food allergies. It’s also important in the absorption of calories into the body, and thus its overgrowth is linked to obesity.

Increasing levels of bacteroidetes may be able to prevent or reverse obesity, but it should also be considered that it’s implicated in the symptoms of irritable bowel diseases like Crohn’s and Colitis. Patients with Crohn’s and Colitis have been found to have disproportionately high levels of bacteroidetes to firmicutes.

This could be for one of several reasons. The role of antibiotics is heavily implicated in IBD, and it’s been shown that after a course of antibiotics bacteroidetes is often the prominent survival after a major die-off of the diversity of gut bacteria. Many Crohn’s and Colitis patients also reduce their fiber intake as a means of controlling symptoms. What do these two things have in common?

Bacteroidetes can consume the mucosa of its host in order to avoid starvation, making it extremely resilient and hard to kill. When patients take anti-biotics or go on low-carb diets to try to starve off invasive bacteria, there’s a good chance they’re losing other beneficial bacteria like the Firmicutes as well, but they could be causing further harm by an overgrowth of the bacteroidetes.

I want to redact what I said here. There may be a misunderstanding I had, or conflicting information that requires more reading. Bacteroidetes consumes the intestinals mucins of the host, not mucosa. It then produces acids like butyric acid that are condusive to growth and healing of the mucosa. While promoting overgrowth of Bacteroidetes in a fast is not ideal to Crohn’s, the biproducts it creates are helpful. 

The question remains, how do we feed Firmicutes without further increasing our levels of Bacteroidetes? Hopefully I can find an answer – but it’s hard in a world where current literature only cares about increasing Bacteroidetes to cure obesity.

The answer to increasing Bacteroidetes is pretty clear – increase the intake of a diverse array of fermentable plant fibers and resistant starches. Most western diets are very low in this, the only resistant starch most people ever consume is wheat. Include raw, green bananas, plantains, raw or cooked then cooled potatoes in your diet to increase resistant starch intake.

Why you’re probably wasting time working out.

The sad fact is the media has corrupted a lot of the public’s knowledge about how to actually ‘get fit quick.’

Magazines and special programs sold by personal trainers and at-home exercise DVDs are gimmicks designed to make everything look more difficult in order to convince you that there is a secret method to getting in shape, it’s complicated, and only by doing exactly what they say can you achieve it.

Here’s the truth:

  • The best results come from simplicity
  • If you’re spending an absurd amount of time ‘toning’ a single part of your body, either you’re a bodybuilder and you may know what you’re doing, or you’ve been conned into thinking that you need to do this to look better.

You see it floating around your facebook and twitter feeds, the “30 minute squat program” or whatever they call it now. It promises to firm up your legs, develop your butt and shed weight and all you have to do is these 6-10 different leg exercises. Here’s the kicker, if you actually grabbed a barbell and loaded weight on it, you could hit all the same muscles, burn more calories, and be done in about 15 minutes or less and go on to do the rest of your workout.

But I don’t want to lift weights, I’m not looking to get big, just to tone up!

More hogwash misconceptions. Firming or toning up is a result of gaining muscle and losing fat. You’re doing the same thing with your 30 minute squat program, except it takes longer and you see less results. Without eating a massive amount of food and in many cases taking performance enhancing drugs you will never reach a state that you consider to be ‘too big’ or ‘too bulky.’ You will however ‘tone up’ much, much faster with progressive resistance training – that is gradually increasing the amount of weight you can move.

But lifting weights isn’t functional! 

Functional is another bullshit catch word used to make crossfit style training seem special, it’s a gimmick, it’s slander on a form of strength and conditioning training that’s been around for ages and is proven to work. There’s a reason many Olympic cyclists and sprinters squat – because it WORKS. If it wasn’t functional, why would they do it? Any time you’re looking to directly target muscle growth or fat loss, breaking your movements down into the most basic, anatomically efficient movement will simply make your results faster. If you want to worry about function, take a kickboxing class and weight lift on the side.

What I’m trying to tell you is resistance training will give you what your looking for FASTER

And for many people, more comfortably! In order to see progress off cardio one has to maintain a high level of intensity over a long duration of time. To see the same results from, say, squatting? A challenging weight for 10 reps, rest, repeat for 3 sets and go home.


And weightlifters have known this for decades. Many do full body workouts, 3 times a week, an hour or less per session and see great results. Squat, bench, row, and optionally deadlift. No need for side planks, lunges, goblet squats, front squats, kickbacks and all the other nonsense you see in the magazines, you’re just taking longer to isolate individual muscles. By throwing weight on the bar, you FORCE your body to use all those same muscles anyway.

For clarity’s sake the difference between a bodybuilder and a cardio bunny toning:

A body builder has a clear set of goals and they know exactly which body part they’re targeting, and they’re working it HARD with resistance training. Often times this is combined with PEDs as well as heavy strength training and high calorie diet. They’re driven by results that are quite different from those of the casual gym goer who wants to look better for the beach. They’re taking a longer path because they need to in order to target specific body parts and make them look better. Unless you plan on competing on stage there’s no need for this level of time commitment to look good for the beach, and it’s LESS effective on fat burning.

Could Crohn’s and other Auto-Immune deficiencies be caused by neurotransmitter problems?

Disclaimer: I am not a medical professional, all medical information, recommendations, and supplemental advice should be taken as academic interest value alone, and you should consult with a physician before attempting any therapies or treatments you find online. Serious complications, drug interactions and side effects can occur even by using ‘natural’ off-the-shelf solutions.

In recent news, researchers have discovered a link between the brain and the lymphatic system. This is a huge missing link that could connect the brain to many auto-immune issues.

The link between Crohn’s and neurotransmitters was not shaky to begin with, and this may help cement the foundations of a new theory that explains it.

A single case study has been done on a patient that failed to respond to other treatments and was ‘cured’ of his Crohn’s by balancing of his serotonin and dopamine levels.

There are many contributing factors to gut inflammation but we know that catecholamines and serotonin may play an important role in them. The link between hormone levels and disease activity is not to be discounted. We’ve seen the disease triggered by stress, the hormonal changes caused by pregnancy and it often displays itself around or shortly after puberty and has been linked to an acne medication called Acutane that acts on hormonal changes.

I posted recently on the benefits of intermittent fasting as a therapy for Crohn’s, and this further reinforces / explains both the therapy and the theory. Though alternate explanations of the benefits of fasting include gut rest and starvation of invasive gut bacteria, neither would really be true in an intermittent fast where the gut is heavily taxed during the non-fasted period, and gut bacteria would be given ample food to regenerate during this time.

This leaves us with the hormonal response to starvation, a wave of catecholamine production which includes neurotransmitters such as Dopamine.

Proper hormone function relies on a balance of Serotonin to Dopamine, too much of either is bad. It’s likely that in the case of Crohn’s patients they are high on the Serotonin level. Starvation leads to increased dopamine levels, forcing a rebalancing of the two.

Starvation, in and of itself, of course comes with dangers such as malnutrition, electrolyte imbalance etc. The length of time and level of caloric restriction that’s considered safe for a fast is highly debatable, however this new therapy offers a possible treatment for the imbalance that’s directly targeted, and available off the shelf of your local vitamin and health shop.

Table 1

Individual dosing value: milligrams of L-tyrosine/milligrams of 5-hydroxytryptophan*

Level AM Noon 4 PM 7 PM
Level 1 1500/150 1500/150
Level 2 1500/150 1500/150 1000/300
Level 3 1500/150 1500/150 1000/300 1000/300


*The patient also received the following daily dosing values: 1000 mg of vitamin C, 220 mg of calcium citrate, 75 mg of vitamin B6, 400 μg of folate, 4500 mg L-cysteine, and 400 μg of selenium.
It should be noted that there’s still a very real risk of toxicity in this treatment, and I must remind the reader that I am not a medical professional, and all treatments should be done under observation of a medical professional. The levels of b6 and selenium are near the upper threshold of safe-to-consume doses, and serotonin toxicity can be fatal!

That said, if you are truly interested in trying this therapy, talk to your doctor, tell them you want to try it and you’d like them to monitor your blood for healthy levels of the supplements you’re taking and your neurotransmitter levels. Maybe it can work for you too!

The supplements in the Notes section are important to the efficacy of this treatment. These co-factors ensure the proper use of the primary therapy. Though it may be expensive to buy them all separate, I found my own Men’s Multi Vitamin made by Solgar contains close to the levels of all the ingredients:

Vitamin B-6(As Pyridoxine Hcl) 75 Mg 3750%
Folic Acid 800 Mcg 200%
Calcium(As Calcium Carbonate, Glycinate, Citrate) 400 Mg 40%
Selenium(AS L-SELENOMETHIONE) 200 Mcg 286%
Vitamin C(As L-Ascorbic Acid) 400 Mg 667%

You may need to take additional selenium and Vit C or find another vitamin with different proportions, but a well balanced multi may be cheaper than buying each supplement separately (I priced it out at about $60 minimum to get all of them vs. $30 for the multi, but it may work out to be cheaper over the long run to purchase them separate, also more accurate as you can take exact doses of each.)

I am not payed or endorsed by the Vitamin Shoppe or Solgar products in any way, simply posting this as an observation.

Maybe we could soon have an answer to Auto Immune diseases.

Scared to Squat?

It’s been a long time since I’ve posted lifting advice, so I’m coming back with the leg day goodness.

A lot of people are scared of squatting. They’ve convinced themselves they have bad backs or knees and will make them worse by squatting. Unless at some point in your life you actually had a traumatic injury to your back or knees, chances are your back and knee pain are the result of bad posture and improper muscle balances and core, back and leg exercises like squatting and deadlifts could help, more than hurt.

Mistake #1: You’re scared to go too deep.

Proper depth in a squat or the bottom of a deadlift isn’t just about showing off your flexibility. It’s about properly setting up your bio mechanics to lift a heavy weight out of a low position – and in the case of a squat it’s about properly decelerating that weight and loading it onto your joints and muscles in a healthy position. Form is key to safety!

For the squat you should not stop until your butt is under your knees. Failure to do so places sheering forces on your knees as your muscles pull against each other at odd angles to stabilize your hips and knees around a large mass bearing down on them at a strange angle. When you drop fully into the bottom position, the muscles load in a spring-like action that will help you pop back out of the squat. If you can’t do this properly, you’re putting too much weight on the bar!

For the deadlift, many don’t drop their butt low enough at the start of the lift. They break at the hips, lean forward and drag the weight up like a Romanian deadlift or Stiff-Leg deadlift, then wonder why they have no ass! (Guilty as charged, myself.)

Get that ass down low and lift through the legs before you even start pulling with your back to ensure your’re loading your legs right and protecting your back from doing all the work.

Mistake #2: You don’t engage your core properly, you’re leaning forward or you’re hyper-extending. 

The first mistake is the gym rat that has never been given a form diagnostic in their life, they bend forward and arch their lower back out like they’re trying to make their pecs touch their crotch at the bottom of the squat or the start of the deadlift and lift by flexing their rhomboids and curling their back into hyper extension. This is a recipe for a back injury.

The second type is the gym rat that’s been told to arch their back the other direction when lifting heavy, so they hyper-extend like they’re trying to get into a bridge position without engaging their other core muscles. Their ass sticks way out, their belly sticks way out, their abs are complete jelly, their  rhomboids are in full contraction and their back is killing them the next day. From this position your entire chain breaks. Your quads shorten, your hamstrings extend, your glutes deactivate, and your knees will hurt.

Unfortunately some people don’t fully comprehend the Rippetoe explanation of the arched low back and how to properly use intra-abdominal pressure. It’s not all about the back, it’s about a neutral balance of force between the back and abs braced around the pressure created by expanding your lungs with a deep breath. The lordotic curve you see in demonstrations is only half the battle, and if you go too far, it’s just as bad for your back as arching the other way.  In simple terms, too much S curve is just as bad as a C curve.

The goal is to find the neutral sweet-spot, your back should be more or less straight which will produce a slightly pronounced S curve. Your hips should sit in a neutral position so your pelvis neither dips forward nor backward – the waistband of your pants should not dive significantly lower in front than in back.

Experiment with  bracing your back first, then tightening the abs and leaning forward slightly into a neutral position. Then do the opposite, brace your abs first then slowly tighten up your back. Find out what works best for you, I’ve heard that only one way is correct, but I’m a believer that both achieve the same final resting position and neither is special.

What can I do to feel safer about my squatting before I get under the bar?

1. Planks – For both problems – PROPER planks. Learn to suck in your abs and keep your butt from sticking out during a plank. If your abs don’t start to burn you’re not doing it right!

2. Supermans – For those with C curve – This will help you to learn the feeling of the contracted rhomboids

3. Sit-ups – For those with S curve – Strengthen your core, curl into the situp rather than pivoting at the hip.

4. Ab wheel – For both problems – same deal as planks

5. Stretch your quads! – for those with S curve – Tight quads pull your pelvis down, extending your abs, deactivating them, shortening your back muscles and causing knee pain.

6. Strengthen your glutes! – Both – Glute-ham raises, leg lifts, kickbacks, glute-bridges with your feet as far away form your butt as you can get and your legs spread wide. If you suffer from extreme  S-curve you’ll struggle to activate glutes without highly specific glute-targeting exercises. Leaning to bend into the C-curve can help you to activate them until you can adjust to proper, balanced posture.