Dr. Sandra Kaufmann's thoughts on Rapamycin

Supplements
#22

Limiting carbohydrates with a high SFA intake will just increase apoB.
Also only a temporary increase in lipids will still cause damage, but longer term lipids is more important.

#23

This is an interesting question. I take the view that the dynamic equilibrium is key and that any issues from a temporary increase in lipids can be reversed.

#24

scta123
how long was LDL-C elevated?

Probably about 1 1/2 years from the peak to then a sudden drop in a few months.
Will have my new blood results next week and I will post - hoping all is normal and maintaining.

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#25

I would suggest you start with a very low dose for the first couple of weeks. You needs to have your system adjust to taking it and then gradually increase the dosage a little more. Im in the Agelessrx trial and next weekend i’ll begin taking 15MG of the compound formula of Rapa. I started out with 5MG which I was told is about equivalent to 2MG of the generic brand. So I presume 15Mg will put me in the area of what most here are taking. 6MG per week. Thus far no side affects. Also taking 1000 mG Metformin and LDN 4.5MG a day.

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#26

Hi,
I took my first dose of Sirolimus last week, 2mg. I became very ill. Like I had a bad virus. I was really achy. Any suggestions? I’m afraid to take it again. Thanks in advance.

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#27

You probably had a bad virus. You could take 1 mg to see what happens when you are fully recovered. If you still feel ill, then I would assume it is the Rapamycin, and it may not be suitable for you.

5 Likes
#28

On pages 34 to 36, she cites the studies on which she bases her conclusions regarding hippocampal neurons and sarcopenia. The studies involve long-term chronic use, not pulsed use. Still, she prefers not to recommend it. She does not state it, but I believe it has to do with the mechanism of action. If it is only mTOR inhibition, you have metformin for that.

She posts her scoreboard of supplements she has evaluated. Metformin is the heavy hitter, with high scores on all categories.

METFORMIN KAUFMANN NUMBER: 3.1.3.2.2.2.3

General Information

Earlier use of the base plant, Galega officinalis or the French Lilac, was documented in Medieval Europe as an herbal remedy for diabetic symptoms.

Metformin was officially discovered in 1922. Human studies didn’t begin until the 1950s, however. It was then that the French physician Jean Sterne introduced the substance to her countrymen as a prescription medication in 1957. The compound debuted in the United States in 1995. Presently, up to 150 million people are on the agent.

Interest in the medication as an anti-aging agent was peaked by a study released in 2014. Type 2 diabetics on either metformin or sulfuronureas (a different type of glucose controlling agent) were retrospectively compared with non-diabetics on neither of these drugs. Comparing 150,000 people, the type 2 diabetics on metformin had higher survivability. Let me rephrase…The diabetics did better than non-diabetics. In fact, among patients in their 70’s, mortality was reduced by 15% in the metformin group.

Composition: Metformin is a biguanide (N,N-Dimethylimidodicarbonimidic diamide), also known by the trade name Glucophage.

Stats
Prescription medication: Oral bioavailability: 50-60%.
Peak plasma concentrations: 1 to 3 hours immediate release / 4-8 hours with extended-release formulations.
Uptake can be delayed 30 minutes if taken with food.
Protein binding in plasma: Minimal.
Half life: 1.7 to 4.5 hours

Categories
1 DNA Alteration: 3
•Epigenetic modular; it induces genome-wide DNA methylation
•Modulates the activity of S-adenosylhomocystein hydrolase, an enzyme in the methylation cycle.
•Decreases genomic instability.
•Stimulates telomeric length

2 Mitochondria: 1
•Activates endogenous antioxidants: heme-oxygenate-1, glutamate cysteine ligase, glutathione S-transferase, glutathione peroxidase, SOD, catalase, sulfiredoxin and thioredoxin.
•Works through the Nrf2-ARE pathway (nuclear factor-like 2 - Antioxidant Response Elements).

3 Aging Pathways: 3
•AMP KInase activator.
•Depresses MTOR pathway.

4 Quality control: 2
•Increases DNA repair efficacy.

5 The Immune system: 2
•Blocks the activity of the transcription factor nuclear factor-kB (NF-kB).
•Inhibits the differentiation of monocytes to macrophages.

6 Individual cell requirements: 2
•Boosts the formation of new nerve cells.

7 Waste management: 3
•Reduces blood glucose.
•Reduces AGE formation.
•Slows lipofuscin accumulation.
•Benefits the Cardiovascular system.
•Cancer reduction.
•Delays menopause in female mice.

Side Effects
•The side effects are generally not too bad; GI upset, transient diarrhea, abdominal pain, cramps and excess gas.
•Worst case scenario: Lactic acidosis. 3 cases/100,000 patients.
•Factors that increase this risk include age greater than 60, decreased liver, kidney or cardiac function, diabetic ketoacidosis, surgery, respiratory failure, ethanol intoxication and fasting.
•The drug blocks the metabolism of a few vitamins, so long term therapy should be accompanied by the addition of supplemental B12 and folate. (Take your vitamins).

The score is based on her seven tenets.

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#29

Below is a transcript of a podcast with Sandra Kaufmann as interviewee.

Scroll down.

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#30

I think Sandra Kaufmann is quite good. As people may know my view is that key drivers of aging rest around gene expression, but there are lots of things upstream of that.

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