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I have just done a Intestinal Permiability Urine Test with ARL pathology.
The results are as follows:
Lactulose Recovery: 0.26% – (< 0.30)
Mannitol Recovery: 9.1% (Malabsorbtion) – (9.5 -25.0)
Lactulose:Mannitol Ratio 0.028 – (< 0.035) So it is basically saying i have malabsorbtion which i was suspecting. It says low mannitol is indicative of malabsorbtion. Lactulose and laculose:mannitol ratio seem normal so intestinal permiability “leaky gut” isn’t that much of a factor Other quick info: Im 20, i have chronic fatigue/feeling weak, muscle weakness/lack of strength/muscle loss, water retention at times, poor appetite, sense of touch reduction, poor erections/premature ejaculation, cold hands and feet at times. Weight goes around waist very easily even while trying to have a good diet and exercise and not eating very much for someone of my size. Elevated T.S.H 5.7, Free T4 14.0 (10 – 20), Really high thyroid peroxidase antibodies 2069 should be under 50, low testosterone 10.1 (10.0 – 28.8), Low IGF-1 33.5. DHEA’s low. Low morning cortisol saliva 5.0 (5.5 – 65.0) I have a CD4:CD8 Ratio of 0.8 (1.2 – 3.0) which is low.
My CD8 T-suppressor cells are elevated.
My Hla Class II cells are also elevated.How exactly would low thyroid cause malabsorbtion and what are other hormonal factors that can cause malabsorbtion of nutrients?
I am taking probiotics VSL which is 450 billion good bacteria per serve, L-Glutamine, Vegetable Digestive Enzymes and swedish bitters at times for digestion.
One simple way of thinking about it is that thyroid hormone increase cellular activity by triggering the enlargement and multiplication of mitochondria. Cells – such as those of the gut – can become a lot more active in absorbing substances when they have larger mitochondria to generate much more energy in the form of ATP. Thus without thyroid hormone, everything works a lot slower.
Once the t-3 goes into the mitochondrion does there have to be proper functioning of the mitochondrion to care out the thyroid signaling from t3. One needs t3 to make the cellular energy work, but if the cellular is not up to optimal capacity then one would not get the desired from thyroid hormone. When you are referring to thyroid signaling are you referring to it on a receptor level or deeper with in the energy systems. If a person had a mitochondrial imbalance and t-3 was given with no response could make Dr think by giving more is going to resolve the issue when the real problem is at the cellular level? What is your opinon about giving substrates to help to support mitochondrial function such as ubquinol, acetly carnitine, citrates, iron to help make the ATP? In studies I have come across people with low thyroid hormones are also low in co-enzyme Q10 and iron, b-12. If these are low could it affect the cellular signaling of the thyroid medicine?
So to summarize thyroid start to finish
1. Thyroid Absorption in to the blood
2. Thyroid conversion t-4 to t3
3. Thyroid receptor activation
4. Thyroid cellular signaling to make ATP.So when a person that actually goes to see a traditional thyroid dr they are only looking at really 25% of the equation and leaving out the other 75%. These drs are totally ignoring the factors are what are effecting each one of these stages. When I have time I will sit down and break each one of these down with what factors are affecting them. It should make a good sticky as well.
@hardasnails1973 654 wrote:
Once the t-3 goes into the mitochondrion does there have to be proper functioning of the mitochondrion to care out the thyroid signaling from t3. One needs t3 to make the cellular energy work, but if the cellular is not up to optimal capacity then one would not get the desired from thyroid hormone. When you are referring to thyroid signaling are you referring to it on a receptor level or deeper with in the energy systems. If a person had a mitochondrial imbalance and t-3 was given with no response could make Dr think by giving more is going to resolve the issue when the real problem is at the cellular level? What is your opinon about giving substrates to help to support mitochondrial function such as ubquinol, acetly carnitine, citrates, iron to help make the ATP? In studies I have come across people with low thyroid hormones are also low in co-enzyme Q10 and iron, b-12. If these are low could it affect the cellular signaling of the thyroid medicine?
So to summarize thyroid start to finish
1. Thyroid Absorption in to the blood
2. Thyroid conversion t-4 to t3
3. Thyroid receptor activation
4. Thyroid cellular signaling to make ATP.So when a person that actually goes to see a traditional thyroid dr they are only looking at really 25% of the equation and leaving out the other 75%. These drs are totally ignoring the factors are what are effecting each one of these stages. When I have time I will sit down and break each one of these down with what factors are affecting them. It should make a good sticky as well.
Its probably the fact that without the proper nutritional support and nutrients in the body you can have adverse effects with thyroid hormone replacement (arrithymias etc..)
It is my understanding that Low mitochondrial functioning is probably due to low thyroid hormones to a large degree and lack of nutrients so thyroid replacment and nutritional support would work well for the person as long as cortisol isn’t low. If low as we all know you’d add HC or cortef.
Dr Mariano explained it pretty well once again.
This looks like it will be a great board.
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