Dr. Tyna Moore · 2026-07-09 · Tyna Moore (host), Ksenia Petrushkina
The Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Petrushkina
32 research-tied claims examined: 4 contradicted 1 overstated 1 context 21 supported 5 unverified
4 Contradicted by research
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.
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.
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.
- contradicts: Systemic anticancer therapy in gynecological cancer patients with renal dysfunction. (International journal of gynecological cancer : official journal of the International Gynecological Cancer Society 2007) · cited 48x in the literature
"We review 17 medications that need dose adjustment (cisplatin, carboplatin, doxorubicin, epirubicin, cyclophosphamide, ifosfamide, topotecan, irinotecan, etoposide, capecitabine, bleomycin, methotrexate, actinomycin D, granulocyte-macrophage colony-stimulating factor, metoclopramide, cimetidine, and diphenhydramine) as well as 27 drugs that do not (paclitaxel, docetaxel, pegylated liposomal doxorubicin, gemcitabine, oxaliplatin, fluorouracil, vincristine, letrozole, anastrozole, tamoxifen, leuprorelin, megestrol, gefitinib, erlotinib, trastuzumab, leucovorin, granulocyte colony-stimulating factor, erythropoietin, ondansetron, granisetron, palonosetron, tropisetron, dolasetron, aprepitant, dexamethasone, lorazepam, and diazepam)." (abstract, passage verified)
pubmedfull study (doi) - contradicts: Current Endocrine Therapy in Hormone-Receptor-Positive Breast Cancer: From Tumor Biology t… (Medicina (Kaunas, Lithuania) 2025) · cited 14x in the literature
"In postmenopausal patients with HR-positive, HER2-negative breast cancer with a low recurrence risk, the first line of treatment is usually a standard 5-year period of treatment with aromatase inhibitors (AIs)(letrozole, anastrozole, or exemestane)." (abstract, results, passage verified)
pubmedfull study (doi)
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.
- contradicts: Heart Disease in Women: Unappreciated Challenges, GPER as a New Target. (International journal of molecular sciences 2016) · cited 21x in the literature
"Further, our most recent studies have identified that GPER activation is an important regulator of low density lipoprotein (LDL) receptor metabolism and that expression of the hypofunctional GPER genetic variant is an important contributor to the development of hypercholesterolemia in women." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Estrogen deprivation induces hepatic inflammation, Indoleamine-2,3-dioxygenase 1, tryptoph… (Scientific reports 2026) · cited 2x in the literature
"OVX animals gained more weight and developed an atherogenic plasma profile with increased LDL and total cholesterol and reduced HDL levels compared to intact female animals, which was reversed by estradiol (E2) administration. Ovariectomy results in elevation of hepatic pro-inflammation cytokine (e.g. TNFα, IL6), tryptophan catabolic enzymes (e.g. IDO1, and TDO2) and reduced reverse cholesterol associated gene SR-BI expression and E2- administration also suppressed the ovariectomy-induced hepatic inflammation resulting in reduction of TNFα, IL6, IDO1 and TDO2 while elevation of SR-BI expression." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Estrogen deficiency-induced lipid dysregulation in menopause: Mechanisms, metabolic conseq… (The Journal of steroid biochemistry and molecular biology 2026)
"This review synthesizes current evidence on the pathophysiological mechanisms linking estrogen deficiency to lipid dysregulation in menopause, encompassing alterations in LDL and HDL metabolism, triglyceride accumulation, changes in lipoprotein lipase (LPL) activity, hepatic lipid accumulation, and the roles of estrogen receptor signaling in adipose tissue and liver." (abstract, results, passage verified)
pubmedfull study (doi)
Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.