Todd Allen

I suppose in my unspoken gloating that despite or perhaps because of my diet rich in saturated fat and salt I have no hypertension, inflammation or joint pain I came across as sarcastic. But I had severe salt sensitivity with inflammation, joint pain and many other issues when I ate a HCLF vegan diet. In my case I think it was a side effect of hyperinsulinemia as documented in this review article: The Antinatriuretic Effect of Insulin: An Unappreciated Mechanism for Hypertension Associated with Insulin Resistance? And what is even funnier, the author of this article, George Bakris, was the specialist I was sent to for severe hypertension for which my PCP was unable to find any combination of medications to manage my blood pressure a few years after this article was written. Bakris also failed to manage my blood pressure, he only considered drugs and thought my diet was healthy. A couple years later about the time I joined this forum, just after a friend my age also with Kennedy's Disease died from a stroke prompting me to fire my docs and find my own answers, I came to suspect the problem was my high carb diet and I changed it. Now I don't take any meds at all and often a teaspoon of salt with meals and my resting BP is rarely above 100/60.

Dean, my condolences, that sounds awful. What do you think is causing salt intolerance, genetics, lifestyle or just simply getting old?

Yes, I misspoke earlier this ratio does not directly give free %, indicator of bioactive percent is the appropriate phrasing. There are 6 IGF binding proteins although they also bind IGF-2 and I think a little insulin but IGFBP-3 is the primary binding protein in circulation much more than all of the others combined.

Just went and looked up the real numbers: IGF-1 7,649 daltons IGFBP-3 28,806 daltons So multiply your result by 3.766 to correct for mass and we get 13.416% free IGF-1

IGF-1 is a peptide hormone of about 70 amino acids. The binding proteins are much bigger roughly 200 to 300 amino acids. Thus the ratio of molecules might be nearly 4 times higher than your ratio of masses. Thus I guesstimate your free IGF-1 to be roughly 12%.

I think the problem is the concept. The ratio of how many molecules is of more interest than the ratio of masses of the two substances. IGF-1 is small, the binding protein much larger.

ALP is typically in a metabolic panel and not a CBC. When part of these panels it will be the basic test 84075. 84080 adds an additional step of electrophoresis to stratify the isoforms. IAP is present in each. That you refer to serum AP as it were some type of AP and having informed us it is found in the blood as if the definition of serum was not the liquid part of the blood makes a terrible impression...

Mike, open your eyes and use them to read medical text books. You didn't even know that intestinal alkaline phosphatase is present in serum tests of alkaline phosphatase.

You can find the same info in Harrison's Principles. Numerous liver conditions can cause 2X the UL for ALP and alcohol is a potential cause of those conditions. I'm not interested in hacking this. I'm trying to help you see the Levine biological age formula is disconnected from reality and should not be used the way you are using it. Another example, ALP is highest in our youth it does not linearly increase with age. A given value tells you nothing about your age.

Might try converting each to mmol/L and then take the ratio.

001612: Alkaline Phosphatase Isoenzymes | Labcorp https://www.labcorp.com/tests/001612/alkaline-phosphatase-isoenzymes Liver is the isoenzyme most frequently elevated when total ALP levels are elevated. Liver ALP increases in the blood early in liver disease before most other liver function tests show abnormalities. The wide group of conditions leading to increased liver ALP include acute hepatitis, cirrhosis, fatty liver, Those can each be caused by excess alcohol consumption. And a 25 point increase in ALP is tiny so it would only take the earliest stage of disease to produce it. But let's assume from your reference that moderate consumption lowers ALP. In that case we can correct an elevated ALP by moderate drinking which still is unlikely to actually be reducing biological age.

We can look at text books for alk phos and find a large number of things which are bad that lower it and a large number of things which are bad that raise it. We don't need research to show exact amounts by which these things do so to recognize that a given value or change in values is meaningless without the context of the causes for that resulting value. And yes there is a possibility that another biomarker might change in a way that compensates for this ones failure. But they might also exaggerate the problem as the other biomarkers also have problems. For example, the anorexic woman has very little muscle mass so her creatinine was also too low but the drinking aggravates her early stage kidney disease optimizing her creatinine in addition to her alk phos.

An anorexic woman with malnutrition induced alk phos of 25 takes up drinking to bring it up to 50 and optimize her biological age...

Yes and this good thing increasing IAP in the intestines will increase slightly serum alkaline phosphatase, moving it in the same direction as a bad thing, intestinal cellular damage resulting in increased rate of IAP leakage. Alkaline phosphatase includes enzyme from liver, bones and other tissues and there are good and bad things that lower each isoform and good and bad things that raise each isoform. It is wrong to state that an alk phos of 40 is some amount more desirable/younger then of 45. Only for a population in a statistical sense are there optimal values. On an individual basis context matters. Most if not all of the biomarkers used in the biological age formula suffer from similar problems. Tests are included in standardized panels because they are easy/cheap to do not because they are the best or even good.