HoldsUp

Ksenia Petrushkina

Dr. Ksenia Petrushkina is a medical professional specializing in regenerative medicine. Her focus centers on longevity, hormone replacement therapy, GLP-1s, peptides, and the role of lifestyle and muscle maintenance in healthy aging. No published research is listed for her in the provided records.

24 claims checked on air: 1 context 4 contradicted 1 overstated 15 supported 3 unverified

What they said on air - contradicted

0:24:36contradictedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Thymosin alpha-1 is approved as a medication throughout Europe.

"And Thymosin alpha has been approved all over the Europe." (said at 0:24:36)

The claim that Thymosin alpha-1 has been approved all over Europe is contradicted by published records of its regulatory and commercial development. While synthetic thymosin alpha-1 (thymalfasin/Zadaxin) has been approved by regulatory agencies in numerous countries outside Europe (such as in Asia and Latin America for hepatitis B and immune enhancement), its commercial development rights specifically excluded Europe and the United States, and it lacks standard regulatory approval across Europe.

0:33:32contradictedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Hormone pellet implants are not FDA-approved.

"Plus, it's not FDA-approved. Where are the studies? I didn't see much." (said at 0:33:32)

The claim that hormone pellet implants are not FDA-approved is contradicted by published literature. While many compounded bioidentical hormone pellets (such as custom estrogen or testosterone formulations, or compounded testosterone pellets like E100) are non-FDA-approved compounded products, branded testosterone pellet therapy (Testopel) has been FDA-approved in the United States since 1972 for male hypogonadism. Furthermore, numerous published studies evaluate both FDA-approved and compounded pellet formulations.

0:36:20contradictedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Anastrozole is a chemotherapy medication that is toxic to the kidneys.

"And by the way, anastrozole is a chemotherapy drug that your kidney hate, but who cares because, you know, you're on a cycle." (said at 0:36:20)

The speaker's statement contains two major factual errors. First, anastrozole is not a chemotherapy (cytotoxic) drug; it is a non-steroidal aromatase inhibitor classified as endocrine (hormone) therapy, primarily used in hormone receptor-positive breast cancer to suppress estrogen synthesis. Second, anastrozole is not recognized clinically as a nephrotoxic medication. Because it is primarily eliminated through hepatic metabolism and less than 10% is excreted unchanged in urine, standard oncologic guidelines do not require dose adjustments for renal impairment, contrasting sharply with known nephrotoxic anticancer agents.

0:49:48contradictedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Cholesterol levels rise in perimenopause because the liver continues producing cholesterol to synthesize steroid hormones after the ovaries stop responding.

"So once your ovaries give out, your body cannot synthesize hormones anymore. But your liver didn't get the message, so it's going to continue producing cholesterol to make the hormones, but hormones are not being made. And that cycle becomes a vicious cycle of, you know, LDL is over the roof and anything else." (said at 0:49:48)

The speaker's proposed mechanism—that LDL cholesterol rises during perimenopause because the liver continues overproducing cholesterol to supply ovaries that no longer synthesize steroid hormones—is biologically incorrect. Hepatic cholesterol synthesis is regulated locally by intracellular sterol sensing mechanisms (via SREBP-2 and HMG-CoA reductase feedback), not by a compensatory drive to fulfill ovarian hormone production. Published research demonstrates that the rise in circulating LDL cholesterol during the menopausal transition is primarily driven by the loss of estrogen-dependent regulation of hepatic lipid metabolism, notably decreased hepatic low-density lipoprotein receptor (LDLR) expression and impaired LDL particle clearance, along with alterations in reverse cholesterol transport pathways and hepatic inflammation.

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