GFR is the rate of filtration. eGFR is a rate of filtration estimated from another biomarker. This can be creatinine, cystatin-c or a mixture of those and there are other factors that can be taken into account
Here is one example of an online calculator
Creatinine has two big problems. One is that it metabolises in blood samples so the time taken between blood being sampled and the test being done (and the temperature) matters. This is particularly important for samples sent in the post. I estimate it can change by 10 microMolar per day.
The second is that creatinine is sensitive both to exercise and muscle mass.
Cystatin-C does not have those problems.
In fact the ratio of creatinine to cystatin-c is an indicator of health (more creatinine to cystatin-c is good).
Then for each decade they have a longevity score. Basically 0 is you are at the lower end of the longevity range for the decade and 1 is you are at the top of the longevity for the decade.
Here is the 10 year survival vs longevity score for age 60+
And finally each biological marker is normalized to its reference range with the lower values in blue, the intermediate values in white and the high values in red.
Applying that to creatinine we see that for 30’s, 40’and 50’s the creatinine increases with the longevity score so more creatinine is better and the older you get the more creatinine for a longevity score of 1.
Now for 60’s we get a U shaped curve staring white then blue then white/red-ish.
For 70’s we see a totally red start which probably are people with kidney failure followed by a slight U shape again.
So if you look at the normalized reference ranges I posted above. It’s 0.7 to 1.3 for creatinine for males so is seems the sweet spot is around 1 or a little bit higher.
That said these are statistical correlation so this doesn’t tell if there is any causation in any direction.
This is also an average and they don’t give the confidence interval so this only works at a population level not for any particular individual.
I’m a little slower than most so forgive the possibly dumb questions.
For LDL it looks like in your 30’s low LDL is a bad thing? In the 50’s and 60’s Low LDL is the best possible. In the 70’s I’m going to guess they don’t run the range high enough to get a curve, so you want it above 100? On your list of high and low they list NA instead of 0 for the low end. Why?
Also for vitamin D in 30’s 40’s and 50’s they have it grey’d out. Can you guess what that means?
@Neo thanks. I will try pendulum probiotic. In general I believe that what is best for my health and longevity is metabolic flexibility: the ability to burn fat or glucose, and switch between them quickly, without creating metabolic damage or debris. Keto is not a long term solution for metabolic flexibility although it was very useful to me to help my body relearn to burn fat (and lose my sharp hunger feelings forever).
I’m not sure if it is possible for me to recover my youthful ability to eat pounds of sugar and feel great. But I don’t want to eat sugar anyway. I do want to eat bread and pasta and rice, which I do not eat now.
I can eat whatever I want as long as I exercise immediately afterwards, based on body sensation and CGM. Drugs such as acarbose and Cana are a less attractive but acceptable way to allow me to indulge. For now I am focusing on high fiber foods, low glycemic index foods (except for berries in AM and apples before my workouts), stress mgmt, metformin/ berberine, GLYLO ingredients, etc.
For LDL, you are right that too low LDL is bad. Same for total cholesterol. BTW That’s a common finding of the all cause mortality and centenarian studies.
Also it’s rather flat. On the other hand the HDL has much more predictive power and has a very consistent correlation with the longevity score. Low is bad, high is good.
For vitamin D it’s probably because it was not measured in people below 50.
I’ve started pendulum 1 month ago. I will report how it works on my HbA1C in a few months.
Looking at that plot, glucose is universally always very bad even independently of T2DM.
I’m eating low carbs (not 20g carbs Keto) and my glucose spikes are somewhat moderate. I’ve been using acarbose for months now and that reduces those spikes even more. What I have left now is my own endogenous production by the liver which is too high that’s why I’m trying pendulum as my last attempt before I try some medication like SGLT2 inhibitors.
BTW acarbose is a sugar that does not even go into the body so I don’t consider that as a medication. (low systemic bioavailability - less than 2% gets absorbed as the active drug)
@cl-user Thanks. I have a similar issue: liver puts out too much glucose. It may be genetic but I also believe it is poor stress regulation (which may also be genetic). I am working very diligently on acquiring the skills of a balanced ANS. The 1st thing I’m aiming to collect is longer natural sleep (no chemicals).
Here is another fascinating plot. The previous one was for longevity and this one is for chronic diseases.
Some tips to interpret this:
Bio markers that go from blue to red in a column are very high positively correlated with that disease: The more of it, the more of the disease.
For instance glucose is highly positively correlated with… every disease!
Bio markers that go from red to blue in a column are very high negatively correlated with that disease: The more of it, the less of the disease.
For instance HDL is highly negatively correlated with every disease (That’s the smiley of me having tons of HDL)
Bio markers that stay more or less the same color in a column are not correlated with that disease.
For instance MPV is not correlated to T2D and only slightly positively correlated to COPD.
@cl-user HDL. Niacin was used to increase HDL but was stopped as an intervention when it didn’t reduce events. I wonder if the niacin induced higher HDL is good for all cause mortality and chronic disease as shown on these charts. Have you heard of niacin-induced-higher-HDL being different?
HDL is an indicator of good metabolism but it’s not causal. It’s just that it reflects your metabolism state.
That’s why when Pharma/Supplements have been used to artificially increase that HDL it turned out to not be improving anything much if at all.
This is different from glucose for instance which causes plenty of issues. Though it’s some way some could argue that it’s both a symptom and a cause of insulin resistance.
There may be a promising path to drug the metabolism and achieve those types of positive longevity, cardiovascular, neurological health benefits
One example that seems to have some promise:
At NewAmsterdam Pharma, we are passionate about providing transformational therapies for patients suffering from an array of conditions where aberrant cholesterol metabolism
Our lead investigational candidate, obicetrapib, is a novel, selective inhibitor that targets the Cholesteryl Ester Transfer Protein (CETP), which has been shown in clinical trials to significantly reduce low-density lipoprotein cholesterol (LDL-C) while at the same time substantially increase high-density lipoprotein cholesterol (HDL-C)
CETP functions to transport cholesterol from good HDL to bad LDL. Obicetrapib works by blocking this transfer, thus substantially lowering LDL while simultaneously increasing HDL. We believe by transforming the ratio of good versus bad cholesterol in the body, obicetrapib holds transformative treatment potential for patients.
ROBUST GENETIC MECHANISM. Blocking CETP exhibits a strong genetic linkage to human metabolic diseases. CETP loss of function is +considered a longevity gene*, and people with CETP loss of function have been observed to be significantly less likely to develop metabolic diseases, such as coronary artery disease, diabetes, and Alzheimer’s disease.
After success phase 2 trials it’s now in several phase 3 trials
For example, high creatinine
and alanine transaminase (ALT) levels are linked to an elevated risk for
CKD and LD, respectively, for patients at any age, as expected. More
surprisingly, their correlation with the lifelong risk of other diseases is
inverted in middle age
Curious about ALT. However, it is quite obvious that Creatinine is in part driven by muscle mass and frailer people as they get older are more likely to die.
With regard to eGFR, there is a new test under development: SDMA. And it might provide the best measure of kidney function. The test itself is available through Labcorp, but a corresponding formula for eGFR has not yet been agreed on. Yale researchers were working on that in cooperation with laboratories. For now, the test can still be ordered with a numerical value and a cutoff for out-of-range. It’s been in use in veterinary practice already for a while now.
People with a significant ongoing discrepancy between cystatin C and creatinine-based eGFR values (where one is out of range and the other isn’t), may wish to consider having a uACR test done.
The SDMA test is paired with ADMA, and elevated ADMA is associated with a higher risk for atherosclerosis.
(That’s the smiley of me having tons of HDL)
