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X-Batch-Id: 1843f63d-9f35-4bb6-a936-0fe5fce0ac8c X-Subscriber-ID: 9c40d639-6e1d-4292-a9d7-0e4cbbb5d5db sId: fd41630e-e91f-46d9-a274-b740dab756d2 x-beehiiv-ids: {"account_name":"https://huntershealthhacks.beehiiv.com/","campaign_id":"4a19b723-fa70-482f-8542-b06a7a758d16","category":"newsletter","email_generated_at":1774476373,"user_id":"fd41630e-e91f-46d9-a274-b740dab756d2"} x-beehiiv-type: newsletter x-list-id: fd41630e-e91f-46d9-a274-b740dab756d2 x-list-owner: x-newsletter: https://huntershealthhacks.beehiiv.com/p/hgh-peptides-cause-cancer x-newsletter-id: https://huntershealthhacks.beehiiv.com/ x-newsletter-signup: https://huntershealthhacks.beehiiv.com/subscribe Mime-Version: 1.0 Date: Wed, 25 Mar 2026 22:06:15 +0000 Message-ID: <20260325.220615.743fa23f@mta37> --ZRvSqzs8TyGGrG5MOuwgAQ Content-Type: text/plain; charset="utf-8" Content-Transfer-Encoding: quoted-printable Happy Wednesday!=0A=0AI was recording a podcast yesterday with one of the t= op cardiologists in the country, who is also a huge proponent of peptides (= stay tuned, as I will be releasing it soon).=0A=0AHe referred me [to a stud= y](https://insight.jci.org/articles/view/140134) that evaluated tesamorelin= on liver health.=0A=0A=0AJCI Insight -=0AEffects of tesamorelin on hepatic= transcriptomic signatures in HIV-associated NAFLD=0A: (https://insight.jci= .org/articles/view/140134)=0A=0ABut in the study, they uncovered something = VERY interesting regarding HGH and cancer risk.=0A=0AYou've probably heard = it a hundred times. Growth hormone causes cancer. IGF-1 feeds tumors. If yo= u touch the GH axis, you're playing with fire.=0A=0AI've always had questio= ns about that framing. Not because I ignore the concern. But the blanket st= atement never sat right with me.=0A=0AAnd today, I=E2=80=99ll walk you thro= ugh the study that actually went inside the liver and looked at what happen= s at the gene expression level when you use tesamorelin for 12 months.=0A= =0AWhat they found should change the conversation, especially for anyone us= ing or considering tesamorelin and/or other GH peptides.=0A=0A=E2=80=94=E2= =80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80= =94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94= =E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2= =80=94=0A=0A**The Study**=0A=0AThis paper was published in JCI Insight in 2= 020.=0A=0AThe research team was led by Steven Grinspoon and Raymond Chung a= t Massachusetts General Hospital and Harvard Medical School. These are seri= ous researchers with decades of work in metabolic disease and hepatology.= =0A=0AThey ran a randomized, double-blind, placebo-controlled trial in peop= le living with HIV who also had non-alcoholic fatty liver disease (NAFLD). = One group got tesamorelin 2mg daily. The other got a placebo. For 12 months= .=0A=0ABut the part that makes this study unique is what came next. They to= ok paired liver biopsies. One at the start. One at 12 months. Then they ran= a full transcriptomic analysis on the tissue. Meaning they looked at the e= xpression of every gene in those liver samples.=0A=0A=E2=80=94=E2=80=94=E2= =80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80= =94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94= =E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=0A= =0A**What They Found About Cancer-Related Genes**=0A=0AThis is where it get= s interesting.=0A=0AThe researchers used curated gene sets that predict out= comes in hepatocellular carcinoma (HCC), which is liver cancer. These gene = signatures have been validated in prior research to correlate with either a= favorable or a poor cancer prognosis.=0A=0ATesamorelin upregulated the gen= es associated with a favorable HCC prognosis. And it downregulated the gene= s associated with poor HCC prognosis.=0A=0ARead that again. The gene expres= sion profile shifted _toward a protective pattern_ against liver cancer. _N= ot a promotional one._=0A=0AThe favorable genes that went up were mostly no= rmal liver housekeeping functions. Bile acid metabolism. Detoxification enz= ymes. Transport proteins. Lipoprotein metabolism. These are signatures of a= healthy, well-functioning liver.=0A=0AThe unfavorable genes that decreased= included hepatic stellate cell activation markers and fibrogenic growth fa= ctor signaling, such as PDGFRB and HGF. These are the genes you don't want = turned on because they're associated with fibrosis progression and cancer d= evelopment.=0A=0A=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2= =80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80= =94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94= =E2=80=94=E2=80=94=E2=80=94=E2=80=94=0A=0A**Cell Division**=0A=0AFour major= gene sets involved in cell proliferation were suppressed by tesamorelin co= mpared to placebo.=0A=0AThese included G2M checkpoint genes, E2F targets, m= itotic spindle assembly genes, and KRAS signaling. The proliferation marker= Ki-67 (MKI67) was also downregulated.=0A=0AIf you're not familiar with the= se pathways, here's the simple version. Uncontrolled cell division is one o= f the fundamental hallmarks of cancer. Every oncology textbook starts there= . Cells that won't stop dividing eventually form tumors.=0A=0ATesamorelin d= idn't accelerate cell division. It slowed it down.=0A=0AThe researchers als= o found that minichromosome maintenance genes MCM2 and MCM6 were downregula= ted. These specific genes have been shown in separate studies to be elevate= d in liver cancer and associated with worse survival outcomes.=0A=0A=E2=80= =94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94= =E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2= =80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80= =94=E2=80=94=0A=0A**The Inflammation and Fibrosis Connection**=0A=0AFive in= flammatory gene pathways were suppressed by tesamorelin. These included TNF= -alpha/NF-kB signaling and IL-6/JAK/STAT3 signaling.=0A=0ABoth of those pat= hways are heavily implicated in the progression from chronic liver inflamma= tion to liver cancer. The inflammation-to-cancer pipeline in the liver is w= ell documented. Reduce inflammation, and you reduce one of the major driver= s of cancer risk.=0A=0AOn top of that, tesamorelin downregulated TGF-beta s= ignaling and epithelial-mesenchymal transition (EMT). EMT is a process in w= hich normal cells begin to behave like mesenchymal cells. =0A=0AThis is a k= ey mechanism in cancer metastasis and progression. TGF-beta is the master r= egulator of fibrosis and also drives cancer progression.=0A=0ATesamorelin a= lso suppressed the YAP/TAZ signaling pathway. YAP/TAZ is a well-documented = driver of both fibrosis and carcinogenesis in the liver.=0A=0AEvery single = cancer-relevant pathway they measured moved in the favorable direction.=0A= =0A=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94= =E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2= =80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80= =94=E2=80=94=E2=80=94=0A=0A**But What About IGF-1?**=0A=0AThe authors addre= ssed the theoretical concern that raising GH and IGF-1 could increase cance= r risk.=0A=0ATesamorelin is a GHRH analog. It doesn't directly inject growt= h hormone. It stimulates your hypothalamus to release GH in a pulsatile pat= tern. The way your body was designed to produce it.=0A=0AWhen you use tesam= orelin, IGF-1 levels rise, but remain within the normal physiological range= . =0A=0AThis is fundamentally different from supraphysiologic abuse of exog= enous GH, where IGF-1 can spike well above normal and healthy levels.=0A=0A= The cancer concern with the GH/IGF-1 axis has always been about chronically= elevated, supraphysiologic levels. Not about restoring normal pulsatile se= cretion. Tesamorelin does the latter.=0A=0A=E2=80=94=E2=80=94=E2=80=94=E2= =80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80= =94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94= =E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=0A=0A**Fina= l Thoughts**=0A=0AI'm won=E2=80=99t sit here and tell you tesamorelin is gu= aranteed to be cancer-free. No compound has that guarantee. And this study = has limitations.=0A=0AThe sample size was small. 18 tesamorelin and 21 plac= ebo participants. The population was HIV-positive with NAFLD, which means w= e can't automatically generalize these findings to otherwise healthy people= . =0A=0AThe study lasted 12 months, which is short relative to cancer timel= ines. And gene expression changes don't always translate directly to clinic= al outcomes.=0A=0ABut here's what I keep coming back to.=0A=0AHarvard resea= rchers took actual liver tissue, ran whole-transcriptome analysis, and look= ed at what tesamorelin was doing at the molecular level. Across every cance= r-relevant pathway they measured, the direction was favorable.=0A=0AOxidati= ve phosphorylation went up. Inflammation went down. Cell proliferation went= down. Fibrotic signaling went down. Cancer-favorable gene signatures went = up. Cancer-unfavorable gene signatures went down.=0A=0ASo the next time you= hear that =E2=80=9CHGH peptides cause cancer!=E2=80=9D just forward them t= his study.=0A=0AAnd more importantly, if you use or are considering using t= esamorelin, know that the real data we have show positive benefits, especia= lly in the context of cancer.=0A=0AThank you for being a reader of my work!= =0A=0ABest,=0A=0AHunter Williams=0A=0A=E2=80=94=E2=80=94=E2=80=94=E2=80=94= =E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2= =80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80= =94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=E2=80=94=0A=0A**Further Re= ading**=0A=0A[_Fourman LT, Billingsley JM, Agyapong G, et al. Effects of te= samorelin on hepatic transcriptomic signatures in HIV-associated NAFLD. JCI= Insight. 2020;5(16):e140134. doi:10.1172/jci.insight.140134_](https://insi= ght.jci.org/articles/view/140134)=0A=0A=0A=E2=80=94=E2=80=94=E2=80=94=0A=0A= You are reading a plain text version of this post. For the best experience,= copy and paste this link in your browser to view the post online:=0Ahttps:= //huntershealthhacks.beehiiv.com/p/hgh-peptides-cause-cancer --ZRvSqzs8TyGGrG5MOuwgAQ Content-Type: text/html; charset="utf-8" Content-Transfer-Encoding: quoted-printable HGH Peptides Cause Cancer?
A critical, evidence-based = analysis  ‌ ‌ ‌ ‌ ‌&= #160;‌ ‌ ‌ ‌ ‌ ̴= 4; ‌ ‌ ‌ ‌ ‌ &#= 8204; ‌ ‌ ‌ ‌ ‌ = ;‌ ‌ ‌ ‌ ‌ ‌&#= 160;‌ ‌ ‌ ‌ ‌ ‌= ; ‌ ‌ ‌ ‌ ‌ = 204; ‌ ‌ ‌ ‌ ‌ = ‌ ‌ ‌ ‌ ‌ ‌= 60;‌ ‌ ‌ ‌ ‌ ‌=  ‌ ‌ ‌ ‌ ‌ R= 04; ‌ ‌ ‌ ‌ ‌ &= #8204; ‌ ‌ ‌ ‌ ‌= 0;‌ ‌ ‌ ‌ ‌ ‌&= #160;‌ ‌ ‌ ‌ ‌ ̴= 4; ‌ ‌ ‌ ‌ ‌ &#= 8204; ‌ ‌ ‌ ‌ ‌ = ;‌ ‌ ‌ ‌ ‌ ‌&#= 160;‌ ‌ ‌ ‌ ‌ ‌= ; ‌ ‌ ‌ ‌ ‌ = 204; ‌ ‌ ‌ ‌ ‌ = ‌ ‌ ‌ ‌ ‌ ‌= 60;‌ ‌ ‌ ‌ ‌ ‌=  ‌ ‌ ‌ ‌ ‌ R= 04; ‌ ‌ ‌ ‌ ‌ &= #8204; ‌ ‌ ‌ ‌ ‌= 0;‌ ‌ ‌ ‌ ‌ ‌&= #160;‌ ‌ ‌ ‌ ‌ ̴= 4; ‌ ‌ ‌ ‌ ‌ &#= 8204; ‌ ‌ ‌ ‌ ‌ = ;‌ ‌ ‌ ‌ ‌ ‌&#= 160;‌ ‌ ‌ ‌ ‌ ‌= ; ‌ ‌ ‌ ‌ ‌ = 204; ‌ ‌ ‌ ‌ ‌ = ‌ ‌ ‌ ‌ ‌
--ZRvSqzs8TyGGrG5MOuwgAQ--

March 25, 2026   |   Read online<= /a>

HGH Peptides Cause Cancer?

A criti= cal, evidence-based analysis

 
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=

Read that again. The gene expression profile shifted toward a protective pattern against liver cancer. Not a promotional one.

<= tr>

Happy Wednesday!

I was re= cording a podcast yesterday with one of the top cardiologists in the countr= y, who is also a huge proponent of peptides (stay tuned, as I will be relea= sing it soon).

He referred m= e to= a study that evaluated= tesamorelin on liver health.

JCI Insight - Effects of tesamorelin on hep= atic transcriptomic signatures in HIV-associated NAFLD

Click here to read the study itself

insight.jci.org/arti= cles/view/140134

<= /td>

But in the study, they uncovered someth= ing VERY interesting regarding HGH and cancer risk.

You've probably heard it a hundred times. Growt= h hormone causes cancer. IGF-1 feeds tumors. If you touch the GH axis, you&= #39;re playing with fire.

I&= #39;ve always had questions about that framing. Not because I ignore the co= ncern. But the blanket statement never sat right with me.

And today, I=E2=80=99ll walk you through the = study that actually went inside the liver and looked at what happens at the= gene expression level when you use tesamorelin for 12 months.

What they found should change the conver= sation, especially for anyone using or considering tesamorelin and/or other= GH peptides.

=
 

= The Study

This paper was published in JCI Insight in 2020.

The research team was led by St= even Grinspoon and Raymond Chung at Massachusetts General Hospital and Harv= ard Medical School. These are serious researchers with decades of work in m= etabolic disease and hepatology.

They ran a randomized, double-blind, placebo-controlled trial in peopl= e living with HIV who also had non-alcoholic fatty liver disease (NAFLD). O= ne group got tesamorelin 2mg daily. The other got a placebo. For 12 months.=

But the part that makes thi= s study unique is what came next. They took paired liver biopsies. One at t= he start. One at 12 months. Then they ran a full transcriptomic analysis on= the tissue. Meaning they looked at the expression of every gene in those l= iver samples.

=
 

= What They Found About Cancer-Related G= enes

This is where it ge= ts interesting.

The research= ers used curated gene sets that predict outcomes in hepatocellular carcinom= a (HCC), which is liver cancer. These gene signatures have been validated i= n prior research to correlate with either a favorable or a poor cancer prog= nosis.

Tesamorelin upregulat= ed the genes associated with a favorable HCC prognosis. And it downregulate= d the genes associated with poor HCC prognosis.

The favorable genes that went up were mostly = normal liver housekeeping functions. Bile acid metabolism. Detoxification e= nzymes. Transport proteins. Lipoprotein metabolism. These are signatures of= a healthy, well-functioning liver.

The unfavorable genes that decreased included hepatic stellate cell= activation markers and fibrogenic growth factor signaling, such as PDGFRB = and HGF. These are the genes you don't want turned on because they'= re associated with fibrosis progression and cancer development.

<= /td>
 

Cell Division

Four major gene sets involved in cell proliferation were suppressed by = tesamorelin compared to placebo.

These included G2M checkpoint genes, E2F targets, mitotic spindle asse= mbly genes, and KRAS signaling. The proliferation marker Ki-67 (MKI67) was = also downregulated.

If you&#= 39;re not familiar with these pathways, here's the simple version. Unco= ntrolled cell division is one of the fundamental hallmarks of cancer. Every= oncology textbook starts there. Cells that won't stop dividing eventua= lly form tumors.

Tesamorelin= didn't accelerate cell division. It slowed it down.

The researchers also found that minichromosome= maintenance genes MCM2 and MCM6 were downregulated. These specific genes h= ave been shown in separate studies to be elevated in liver cancer and assoc= iated with worse survival outcomes.

 =

The Inflammation= and Fibrosis Connection

Five inflammatory gene pathways were suppressed by tesamorelin. These incl= uded TNF-alpha/NF-kB signaling and IL-6/JAK/STAT3 signaling.

<= span style=3D"font-size:1.5rem;">Both of those pathways are heavily implica= ted in the progression from chronic liver inflammation to liver cancer. The= inflammation-to-cancer pipeline in the liver is well documented. Reduce in= flammation, and you reduce one of the major drivers of cancer risk.<= /p>

On top of that, tesamorelin downreg= ulated TGF-beta signaling and epithelial-mesenchymal transition (EMT). EMT = is a process in which normal cells begin to behave like mesenchymal cells. =

This is a key mechanism in = cancer metastasis and progression. TGF-beta is the master regulator of fibr= osis and also drives cancer progression.

Tesamorelin also suppressed the YAP/TAZ signaling pathway. YA= P/TAZ is a well-documented driver of both fibrosis and carcinogenesis in th= e liver.

Every single cancer= -relevant pathway they measured moved in the favorable direction.

 

But What About IGF-1?

The authors addressed the theoretical concern that raising GH= and IGF-1 could increase cancer risk.

Tesamorelin is a GHRH analog. It doesn't directly inject gro= wth hormone. It stimulates your hypothalamus to release GH in a pulsatile p= attern. The way your body was designed to produce it.

When you use tesamorelin, IGF-1 levels rise, but = remain within the normal physiological range.

This is fundamentally different from supraphysiologic ab= use of exogenous GH, where IGF-1 can spike well above normal and healthy le= vels.

The cancer concern wit= h the GH/IGF-1 axis has always been about chronically elevated, supraphysio= logic levels. Not about restoring normal pulsatile secretion. Tesamorelin d= oes the latter.

=

But here's what I keep coming back to.

=
 

Final Thoughts

I'm won=E2=80=99t sit here and tell you= tesamorelin is guaranteed to be cancer-free. No compound has that guarante= e. And this study has limitations.

The sample size was small. 18 tesamorelin and 21 placebo participant= s. The population was HIV-positive with NAFLD, which means we can't aut= omatically generalize these findings to otherwise healthy people.

The study lasted 12 months, which is= short relative to cancer timelines. And gene expression changes don't = always translate directly to clinical outcomes.

Harvard researchers took actual liver ti= ssue, ran whole-transcriptome analysis, and looked at what tesamorelin was = doing at the molecular level. Across every cancer-relevant pathway they mea= sured, the direction was favorable.

Oxidative phosphorylation went up. Inflammation went down. Cell pro= liferation went down. Fibrotic signaling went down. Cancer-favorable gene s= ignatures went up. Cancer-unfavorable gene signatures went down.

=

So the next time you hear that =E2=80= =9CHGH peptides cause cancer!=E2=80=9D just forward them this study.=

And more importantly, if you use o= r are considering using tesamorelin, know that the real data we have show p= ositive benefits, especially in the context of cancer.

Thank you for being a reader of my work!<= /p>

Best,

Hunter Williams

 =

Further Reading<= /b>

Fourman LT, Billingsley JM, Agyapong G, et al. Effects of = tesamorelin on hepatic transcriptomic signatures in HIV-associated NAFLD. J= CI Insight. 2020;5(16):e140134. doi:10.1172/jci.insight.140134

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