[hypoman]

@hardasnails1973 5367 wrote:

As a clinical nutritionist and consultant to many well respected Dr, I have found chasing Rt3 in several cases ended up in failed attempts. In some cases cause more issues. The approach which has worked the best was to find out why your rt3 was high then address it from there. Rt3 is raised by the body for a reason to protect it self. In many cases of rt3 I have dealt with the main reason rt3 was elevated was stress from either the imbalances in the neurology, biology, environmental, nutritional, or genetic factors. All of of these areas need to be explored before IMO putting a person on t3 only. I personally chased Rt3 for years, feeling good then feeling worse never stabilizing. It was not until I goto to the root of the problem did I finally make advances in my health and well being. Just simple nutritional factors where able to resolve many cases, or just healing the GI tract and cleaning out the liver properly. If you are on t4 only, I would look into factors to why t4 was not converting. Then may be suggest 5-10 mcgs BID to help bridge till the main problem was found. Bloods are just a diagnostic tool when most of the real happening its at the intracellular and mitochondial level. One needs to look past the serum. Dr refer cases when all the numbers in blood are fine, cortisol, ferritin, hormones are in check but they can not figure out where else to look. After a while this becomes not only a science, but an art form…

But my main questions are:

1) Is there really any reason to add separate T4 in the case of a depressed free and total T4?

2) In addition to its main function as a storage hormone whose job is to convert to T3, specifically what metabolic or other functions does T4 have and does it really matter if both T4 levels are depressed as long as one is getting enough T3?

[hypoman]

@hardasnails1973 5339 wrote:

Good call !! Why you need to be cautious ….

Reason I do a metametrix Gi effects stool test to confirm this in order to rule it out. One can find a Gi imbalance in about 80% of population even if they are totally asymptomatic. Kind of scary. 30% of people with intestinal hyper permeability issues have no GI related symptoms, but have other symptoms which can be neurological or show in the skin as well as other parts of the body.

Why If I suspect pathogen, lyme, bartonella, mycotoxins or viral load I have Dr vitamin d 1,25 to vitamin D 25 ratio to see if the body is in a pro inflammatory state. This is usually an indirect marker which has been shown to be an excellent indicator

Had client last night from Austrailia as soon as I saw her vitamin D 25 levels , her meds and supplementation, I asked right off the bat if she had vitamin D 1,25 tested. On supplements her vitamin D was 1000 ius which prompted my response. The Drs knew what was going on which was good to hear. Too many Drs over here are cranking vitamin D to 10,000 ius a day. My question is “Is our body lowering vitamin D down to protect us from viral, or pathogen loads?” I am being to believe so…

Even ferritin levels over 220 it will caution a potential red flag for inflammation..

It has long been held that iron supplements feed unfriendly bacteria and protozoan parasites, the hallmarks of dysbiosis. I know Dr. Mariano likes to see a serum ferritin level of between 150-200 for males for proper ATP production & thyroid signaling. In order to reach such levels, exogenous supplementation and/or consuming iron-dense foods such as beef liver are a necessity. Again, my concern is as to “what is a safe threshold”. Also, I believe it is unabsorbed iron that could present more of a potential issue with respect to fueling the growth of gut bugs rather than serum ferritin itself.

However, in this recent study, we have a complete contradiction of this issue – at least in mice: http://www.ncbi.nlm.nih.gov/pubmed/22690070

And this even more recent study suggests that a lower iron intake can facilitate dysbiosis:
http://www.ncbi.nlm.nih.gov/pubmed/22845175

In sum:
“Low Fe conditions (1.56 mg Fe L(-1) ) significantly decreased acetate concentrations, and subsequent Fe supplementation (26.5 mg Fe L(-1) ) restored acetate production. High Fe following normal Fe conditions had no impact on the gut microbiota composition and metabolic activity.”

“The strong dysbiosis of the gut microbiota together with decrease in main gut microbiota metabolites observed with very low iron conditions could weaken the barrier effect of the microbiota and negatively impact gut health.”

Here is some interesting aspects as to iron metabolism:
http://en.wikipedia.org/wiki/Human_iron_metabolism

As to Vit. D being “fertilizer” for known and as-yet unknown pathogens (i.e the so-called nanobacteria), what you say reminds me of the Marshall Protocol which, IMHO, is too radical for me to accept as a rational scientific treatment protocol, especially when it’s based on an unmeasurable “stealth” pathogen:
http://marshallprotocol.com/
http://bacteriality.com/about-the-mp/
http://www.natmedtalk.com/f50/1643-marshall-protocol-stay-away-one.html

Perhaps only in rare maladies such as sarcoidosis would Vit. D be contraindicated.

Speaking of pathogens, specifically Lyme, do you have any knowledge with respect to the CD57 test?

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