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

0:03:50needs contextmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Estrogen, progesterone, and testosterone levels drop in women after ages 40 to 45.

"after 40, 45, we have to take care of our body because estrogen declines, progesterone drops, testosterone drops, everything drops" (said at 0:03:50)

The speaker's general assertion that key female sex hormones decline as women transition through their 40s and into menopause is broadly accurate, but the exact timing and trajectories differ by hormone. Progesterone declines during perimenopause (typically beginning in the 40s) due to an increasing frequency of anovulatory cycles and luteal phase deficiency. Estrogen (principally estradiol) undergoes wide, unpredictable fluctuations during early perimenopause before experiencing a steep and sustained drop in the late perimenopausal transition and postmenopause. In contrast, circulating testosterone declines steadily with age starting in early adulthood (falling by approximately 50% between ages 20 and 40), with relatively modest or stable changes specifically attributable to the menopausal transition itself.

0:06:06supportedmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Using GLP-1 receptor agonists without adequate diet and exercise causes substantial loss of muscle mass alongside fat loss.

"Lose a lot of weight, a lot of muscle, a lot a lot of fat, because nobody educate them that they have to eat, they have to exercise. They can't just take GLP-1 and sit on the couch and watch TV after work. They have to actually gain the muscle." (said at 0:06:06)

Published clinical trials and meta-analyses show that glucagon-like peptide-1 receptor agonist (GLP-1 RA) therapy induces weight loss composed of both fat mass and absolute lean/skeletal muscle mass. A meta-analysis of randomized controlled trials examining GLP-1 RAs at obesity doses found a significant reduction in absolute lean mass (-1.74 kg overall, and -5.44 kg for semaglutide), with lean/skeletal muscle loss typically accounting for roughly 8.5% to 25% (or more) of total weight lost. Clinical guidelines and systematic reviews emphasize that GLP-1 RA pharmacotherapy should be combined with adequate dietary protein intake and structured exercise (especially resistance training) to minimize muscle loss and preserve physical function.

0:08:47supportedmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Muscle mass protects bones from osteoporosis and reduces fracture risk.

"Well, you do need muscle to protect your bones from osteoporosis, as well as protect when estrogen protects you, because muscle feeds the bones. If there's no muscle, your bones are not being fed, and so you're going to break them." (said at 0:08:47)

Prospective cohort studies and systematic reviews demonstrate a robust, positive association between skeletal muscle mass/function and bone health. Sarcopenia (the age-related loss of muscle mass, strength, and function) and osteosarcopenia are significantly associated with reduced bone mineral density (BMD) and an elevated risk of osteoporotic fractures. Meta-analyses show that sarcopenia increases the relative risk of incident fractures (pooled RR ~1.37 to HR ~2.13 in osteosarcopenia), while preserved muscle mass and physical loading stimulate bone remodeling through mechanical tension and endocrine/paracrine signaling (bone-muscle crosstalk).

0:13:44supportedmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Adipose tissue becomes pro-inflammatory when it exceeds a certain threshold.

"Anything above the certain limit becomes an inflammation." (said at 0:13:44)

The speaker's statement accurately reflects the well-established "adipose tissue expandability hypothesis" in metabolic physiology. Adipose tissue depots have an individual capacity limit for healthy expansion. When excess caloric intake exceeds this expansion threshold, adipocyte hypertrophy causes cellular hypoxia, adipocyte death, and immune cell infiltration, triggering chronic low-grade inflammation and the secretion of pro-inflammatory cytokines.

0:15:15supportedmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

There is no safe dose or level of alcohol consumption.

"I'm big proponent of no alcohol at all because there's no safe dosage of alcohol." (said at 0:15:15)

The statement that there is no safe level of alcohol consumption is supported by large-scale global epidemiological analyses. The Global Burden of Diseases (GBD) 2016 study, analyzing data from 195 countries across 23 health outcomes, concluded that the level of alcohol consumption that minimises total health loss is zero standard drinks per week, with cancer risk and all-cause mortality rising monotonically with intake. While subsequent modeling (GBD 2020) highlighted that theoretical minimum risk levels may vary slightly by age and regional baseline disease rates (due to modest reductions in ischemic heart disease risk among older adults), public health authorities and global analyses continue to emphasize that for overall health and cancer risk, no completely safe threshold exists.

0:16:00overstatedmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Alcohol converts to acetaldehyde in the liver, which damages neurons and contributes to neurodegenerative diseases like dementia and Alzheimer's.

"If you look at the uh chemistry of alcohol and as when it converts to, well, your liver, acetaldehyde, it kills the neurons every nanosecond and your liver is trying to detox the acetaldehyde from your blood because it knows your brain is dying slowly. So dementia, Alzheimer's, and all the neurodegenerative diseases, you can prevent that by just not drinking." (said at 0:16:00)

Alcohol is metabolized in the liver to acetaldehyde, a reactive metabolite with well-documented neurotoxic potential through protein and DNA adduct formation, and chronic excessive alcohol intake is an established risk factor for brain damage and dementia. However, claiming that alcohol 'kills neurons every nanosecond' and that 'dementia, Alzheimer's, and all the neurodegenerative diseases, you can prevent that by just not drinking' is vastly overstated. Neurodegenerative diseases like Alzheimer's disease and Parkinson's disease are complex and multifactorial, driven substantially by non-modifiable genetic (e.g., APOE ε4) and age-related factors alongside diverse environmental contributors. Furthermore, epidemiological meta-analyses show that heavy alcohol consumption significantly increases dementia risk, but abstaining from alcohol alone cannot eliminate or prevent all neurodegenerative diseases.

0:21:49supportedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

PT-141 (Vyleesi / bremelanotide) is approved for hypoactive sexual desire disorder in women.

"tried Vyleesi, it is approved for um women hyposexual." (said at 0:21:49)

Bremelanotide (brand name Vyleesi, also known as PT-141) is an FDA-approved subcutaneous melanocortin receptor agonist indicated for the treatment of acquired, generalized hypoactive sexual desire disorder (HSDD) in premenopausal women.

0:22:49supportedvery lowThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

MOTS-c peptide activates AMP-activated protein kinase (AMPK) to regulate energy metabolism.

"That's that's explainable because MOTS-c, it activates AMPK. It reroutes the energy." (said at 0:22:49)

Preclinical studies demonstrate that the mitochondrial-derived peptide MOTS-c acts on cellular energy metabolism by inhibiting de novo purine synthesis and activating 5' adenosine monophosphate-activated protein kinase (AMPK) in skeletal muscle and other metabolic tissues. Because this mechanistic pathway has been characterized primarily in cell culture and animal models, the certainty of evidence for clinical translation in humans remains very low.

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.

0:25:28unverifiedvery lowThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Semax and Selank are available over the counter as nasal sprays in Russia.

"Semax and Selank in Russia, over-the-counter medication. You can just buy the nasal sprays." (said at 0:25:28)

No published record matching the claim that Semax and Selank are approved specifically as over-the-counter medications in Russia was located; this does not prove the claim false. While scientific reviews document that Semax and Selank are synthetic peptide formulations developed in the Russian Federation and commonly administered via intranasal delivery, indexed biomedical literature does not document their precise domestic regulatory prescription status (over-the-counter vs. prescription-only).

0:25:48supportedmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Thymosin beta-4 is a 43-amino-acid peptide being researched in oncology due to its implication in glioblastoma.

"TB4 is what, 43-amino-acid-long peptide, very long peptide that is being researched in oncology because it implicates in glioblastoma." (said at 0:25:48)

Thymosin beta-4 (Tβ4) is an actin-sequestering peptide consisting of 43 amino acids. In oncology research, it has been studied across several cancers, including glioblastoma, where its expression correlates with tumor grade and malignancy. Preclinical research demonstrates that silencing the thymosin beta-4 gene reduces stemness, clonogenicity, invasion, and tumorigenicity in glioblastoma models, leading researchers to explore it as a potential therapeutic target.

0:26:20supportedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

BPC-157 is included on the World Anti-Doping Agency (WADA) prohibited list.

"And it's on the WADA list. BPC-157 is on the WADA list." (said at 0:26:20)

BPC-157 is recognized in the doping control and sports regulatory literature as a prohibited substance under World Anti-Doping Agency (WADA) regulations (specifically added under category S0: Non-Approved Substances / peptide categories), and anti-doping analytical workflows routinely screen for it among prohibited doping agents.

0:26:40supportedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

TB-500 is included on the World Anti-Doping Agency (WADA) prohibited list.

"And it's on the WADA list. BPC-157 is on the WADA list." (said at 0:26:40)

TB-500 (a synthetic peptide representing an active region/form of Thymosin beta-4) and Thymosin beta-4 are prohibited substances under the World Anti-Doping Agency (WADA) Prohibited List (under peptide hormones, growth factors, related substances, and mimetics, or non-approved substances). Published anti-doping literature confirms that TB-500 is classified as a banned doping agent under WADA regulations and subject to doping control detection strategies.

0:30:45unverifiedvery lowThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Intravenous administration of 500 to 750 mg of NAD stopped flare-ups in a patient with psoriatic arthritis.

"Also, I have a patient with psoriatic arthritis whom I gave 500 mg of NAD, I think even 750 once for 3 weeks, and his flare-up stopped." (said at 0:30:45)

No published record matching the claim that intravenous administration of 500 to 750 mg of NAD stopped flare-ups in a patient with psoriatic arthritis was located; this does not prove the claim false.

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.

0:33:45supportedmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Compounded hormone pellets can raise female testosterone levels to male ranges around 500 ng/dL, leading to aromatization and high estrogen levels.

"Yes, I have many, actually, women who came to me from other practitioners who would put them on pellets and then their testosterone would be in 500. I mean, it's not a female range. It's a male-range testosterone of 500s. And then it aromatizes, and then your estrogen goes into 500 and you create that inflammation because you flood it with supraphysiological doses of hormones that your body is not used to." (said at 0:33:45)

The speaker's claim that compounded hormone pellets can result in supraphysiological, male-range testosterone levels in women (around 500 ng/dL) and high serum estradiol (estrogen) levels due to aromatization is supported by clinical evidence. A cohort study comparing postmenopausal women using compounded pellet hormone therapy (PHT) to FDA-approved hormone therapy found that women receiving pellets experienced significantly higher mean peak serum testosterone and estradiol levels compared to standard therapies. In the PHT group, peak testosterone reached up to 599 ng/dL (with multiple patients exceeding 400 ng/dL) and peak estradiol reached up to 1,111 pg/mL, demonstrating that compounded pellets frequently produce supraphysiological male-range testosterone concentrations and marked elevations in estrogen in postmenopausal females.

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.

0:36:49unverifiedvery lowThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Excess exogenous testosterone converts to DHT, leading to benign prostatic hyperplasia and hair loss, and aromatizes to estrogen, causing gynecomastia.

"It's going to convert to DHT. It's going to aromatize to estrogen. And then you need now finasteride to bring the DHT down because high DHT equals BPH—that's bad for your prostate, and your hair falls out, and you're going to lose your hair—and anastrozole because you don't want to have man boobs, but your estrogen goes up." (said at 0:36:49)

No published record matching the claim was located; this does not prove the claim false.

0:49:40supportedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

The liver produces approximately 80% of circulating cholesterol in the human body.

"your liver makes 80% of your cholesterol, and cholesterol is made to synthesize hormones." (said at 0:49:40)

The speaker's statement aligns with human physiological principles. Endogenous cholesterol synthesis accounts for approximately 75% to 80% of circulating and total body cholesterol (with the remaining fraction derived from dietary absorption), and the liver serves as the primary site of de novo cholesterol biosynthesis and circulating lipoprotein regulation. Furthermore, cholesterol is the essential biochemical precursor for the biosynthesis of all steroid hormones (including corticosteroids, androgens, and estrogens), as well as bile acids and cell membrane structures.

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.

0:50:44supportedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Therapies that elevate or mimic growth hormone, such as growth hormone-releasing hormone analogues, cause fluid retention and water weight gain.

"when you inject anything that have to do with the growth hormone because the medication in itself will you will gain the water weight." (said at 0:50:44)

Administration of growth hormone (GH), growth hormone-releasing hormone (GHRH) analogues, and GH secretagogues is well-established to induce sodium and fluid retention, leading to extracellular water accumulation and transient water weight gain or peripheral edema. Clinical trials and reviews evaluating GH-axis modulators (including GHRH analogues like tesamorelin and sermorelin) consistently document fluid retention syndromes, peripheral edema, and increases in lean/extracellular body water as classic, dose-dependent pharmacological effects of elevating GH and IGF-1 levels.

0:51:09supportedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Tesamorelin is a growth hormone-releasing hormone (GHRH) analogue that stimulates the pituitary to secrete growth hormone, which causes the liver to release IGF-1.

"Yes, so tesamorelin is GHRH, it's a growth hormone um it's a peptide that stimulate pituitary inside your brain to produce growth hormone. It travels to your liver. Your liver says, 'Oh, I just got GH. I'm going to release IGF-1.'" (said at 0:51:09)

The speaker accurately describes the mechanism of action of tesamorelin and the physiology of the growth hormone-releasing hormone (GHRH) axis. Tesamorelin is a synthetic peptide analogue of GHRH that binds to receptors in the anterior pituitary gland to stimulate the synthesis and pulsatile release of endogenous growth hormone (GH). Growth hormone subsequently acts on target tissues, primarily the liver, stimulating the production and systemic release of insulin-like growth factor 1 (IGF-1).

1:01:17supportedhighThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Plasmapheresis removes coagulation factors and immunoglobulins from the blood.

"Well, all your coagulation factors are removed with plas— plasmapheresis... Immunoglobulins are removed. Clotting factors are removed. Every— you just removed everything." (said at 1:01:17)

Plasmapheresis (therapeutic plasma exchange) separates and removes the liquid portion of whole blood (plasma), which contains circulating plasma proteins including immunoglobulins, immune complexes, complement proteins, and coagulation factors (e.g., fibrinogen, factor V, factor XI, factor XIII). When albumin or saline is used as the replacement fluid instead of fresh frozen plasma, significant temporary depletion of both immunoglobulins and clotting factors occurs, which is well-documented in clinical apheresis literature.

1:03:04supportedmoderateThe Right Way to Use HRT, GLP-1s & Peptides | Dr. Ksenia Pet

Plasmapheresis can be beneficial in ICU patients with severe diseases, such as severe COVID-19 characterized by cytokine flooding.

"plasmapheresis can be very beneficial in ICU patients with severe diseases, with severe COVID, for example, where you flooded with cytokines. I mean, there's there are settings where that procedure can be beneficial" (said at 1:03:04)

Published systematic reviews and meta-analyses support the claim that therapeutic plasma exchange (plasmapheresis) can provide clinical benefit in severe critical illnesses such as severe COVID-19 characterized by hyperinflammation and cytokine release. Meta-analytic evidence indicates that plasma exchange in severe COVID-19 significantly reduces inflammatory markers (such as IL-6, ferritin, and LDH) and is associated with reduced all-cause mortality compared to standard care.

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