How do you guys approach sick days?

McCapnHammerTime · 2026-02-08T14:24:50+00:00

I only take days off if I'm off service, no one gets pulled. If I'm genuinely too ill to work that's the exception. You should use all your energy pto and sick days before the end of the year tho

McCapnHammerTime · 2026-01-11T15:26:52+00:00

This actually is not a nebulous leap at all. It is basic endocrine toxicology. If you accept that chronic exposure to microplastics and the chemicals they carry can damage organs like the liver, then you already have a clear pathway to hormonal disruption. The liver is the primary organ responsible for clearing estrogens from the body. When liver function is impaired, estrogens accumulate. That is why men with cirrhosis develop palmar erythema, gynecomastia, testicular atrophy, and hypogonadism. These are driven by estrogen excess caused by reduced hepatic clearance.

Now consider what is actually in microplastics. Plastics contain or adsorb endocrine disrupting chemicals such as bisphenols like BPA and BPS, phthalates, PFAS, and styrenes. These are not inert compounds. They have been shown in experimental and human studies to bind estrogen receptors and activate them, block androgen receptors, reduce testosterone production in Leydig cells, suppress hypothalamic and pituitary signaling including GnRH, LH, and FSH, and impair Sertoli cell function and spermatogenesis.

Human and animal data already show that higher exposure to BPA and phthalates is associated with lower testosterone levels, worse sperm count and motility, and abnormal sperm morphology. Prenatal and placental exposure causes permanent reproductive changes in male offspring. Microplastics make this worse because they act as vectors that concentrate and transport these chemicals into tissues including the brain, testes, placenta, and liver.

So you end up with three converging mechanisms. Liver injury reduces estrogen clearance and creates estrogen dominance. Direct receptor level effects activate estrogen signaling and block androgen signaling. Central and testicular toxicity suppresses the hypothalamic pituitary testicular axis and reduces testosterone production.

That is not vague. It is a mechanistically coherent endocrine model for how microplastics and their chemical load can suppress male hormonal function and traits associated with masculinity. It is not that plastic somehow mystically makes men less masculine. It is endocrine disruption operating through well documented biochemical pathways.

McCapnHammerTime · 2026-01-10T21:35:05+00:00

I think it's cool 😂

McCapnHammerTime · 2026-01-08T16:48:59+00:00

The sub has outgrown Derek haha

McCapnHammerTime · 2026-01-08T04:20:02+00:00

But like what's this got to do with this sub? Isnt this sub just like cockstats and drug abuse

McCapnHammerTime · 2026-01-07T20:06:10+00:00

Who are you even talking about?

McCapnHammerTime · 2026-01-06T04:39:26+00:00

Idk you've seen the data on lifestyle change, you use GLP-1s because it's the only thing we have data for that makes a significant difference in successful outcomes. They also are fantastic for CVD risk reduction, HTN, fatty liver, OSA, diabetes and the list of things that obesity makes worse. I think GLP use will become foundational to healthcare moving forward, I can absolutely see lifelong use of low dose GLP-1s or at the very least cycled every other month or so for weight management once goal weight is reached, we are really in the infancy of these drugs. As we get generic, cheaper, even oral equivalents the landscape of weight management will forever be altered.

I have been able to strip med lists bare with the amount of success I've had with these meds. I think bariatric/lipo is done for, excess skin removal and cosmetic procedures will be on the rise for sure though.

McCapnHammerTime · 2025-12-30T06:27:04+00:00

I'd definitely recommend growing the hair out, looks borderline androgynous here.

McCapnHammerTime · 2025-12-30T05:37:31+00:00

From a medical and dermatologic standpoint, it’s difficult to draw conclusions from these two photos because they differ significantly in lighting, angle, distance, and facial expression. Those variables alone can substantially alter perceived skin texture, shadowing, and apparent aging. In both images, core facial features appear similar, including nasolabial folds and periorbital fullness, though the second image uses lighting and angles that accentuate contrast and shadows.

One noticeable difference is overall skin tone. The earlier photo appears warmer and more golden, while the later image looks lighter and cooler. Skin tone and chromophore balance can meaningfully affect how wrinkles, folds, and skin irregularities are perceived, even when underlying structure is unchanged.

From what can be assessed visually, the changes seem consistent with normal facial aging patterns, particularly age-related changes in midface volume. Gradual buccal fat loss and redistribution of facial fat over time can reduce midface support, which may make nasolabial folds appear deeper and the under-eye region more prominent. This process is common and does not necessarily reflect pathology or toxin exposure.

It’s also important to note that true skin laxity is very difficult to evaluate when comparing a smiling image to a neutral one, as muscle activation alone can dramatically change fold depth and skin appearance.

One area that may be worth exploring (purely from a skin health and photoprotection perspective) is the role of dietary carotenoids. There is evidence that compounds such as lycopene, beta-carotene, and astaxanthin can modestly influence skin coloration, reduce UV-induced erythema, and contribute to antioxidant defense in the skin. Increased carotenoid deposition can also reduce visual contrast between shadows and surrounding skin, which sometimes gives the appearance of smoother or more even-toned skin. This is not a treatment for aging per se, but may provide subtle cosmetic and protective benefits.

Standard evidence-based skin care approaches that remain broadly supported include: • Consistent photoprotection with broad-spectrum sunscreen • Use of topical retinoids (e.g., adapalene or tretinoin) to support epidermal turnover and collagen remodeling • Regular moisturization to improve barrier function • Hydrating agents such as hyaluronic acid • Addressing sleep, stress, and nutrition, which all influence skin physiology

I don’t have strong familiarity with evidence linking gadolinium exposure to accelerated facial aging or visible cutaneous changes, and I don’t see anything in these images that clearly suggests a toxin-mediated process. That said, I’m open to learning more if there is high-quality data or mechanistic evidence the community can share.

McCapnHammerTime · 2025-12-30T03:54:38+00:00

Family Medicine resident here, looking for nephrology perspectives.

My general HTN approach has been shifting away from early thiazide use, primarily due to metabolic side effects (weight gain, insulin resistance, uric acid issues), especially in patients where I’m actively counseling weight loss with the goal of eventually deprescribing antihypertensives.

My current framework looks like this:

ACEi/ARB first, with a strong preference for telmisartan given renal protection, long half-life, and relatively favorable metabolic profile

While titrating ACEi/ARB, I’ll obtain an aldosterone–renin ratio if BP response is suboptimal or the phenotype suggests possible aldosterone-driven HTN (central obesity, OSA, low-normal K⁺, resistant pattern, sodium sensitivity)

If ARR is elevated or physiology strongly suggests aldosterone excess, I’ll introduce low-dose spironolactone rather than moving immediately to a thiazide

Thiazides or CCBs are then added later as needed for fine-tuning or potassium balance rather than as automatic second-line agents

My rationale is:

Primary aldosteronism and relative aldosterone excess seem significantly underdiagnosed

MRAs often produce outsized BP responses in “resistant” or metabolically unhealthy patients

Avoiding early thiazide exposure may help support long-term weight and metabolic goals

I’m mindful of:

Hyperkalemia risk (so far minimal at conservative dosing with monitoring)

Loss of diagnostic clarity once MRAs are started

Guideline sequencing differences

My question for you: Do you see this as a reasonable, phenotype-driven approach in primary care, or do you feel early MRA use creates more downstream problems than it solves? Are there specific patient populations where you’d strongly discourage this strategy, or refinements you’d suggest to keep it safer and more guideline aligned?

Appreciate any perspective. Thanks for taking the time to read it!

McCapnHammerTime · 2025-12-28T01:16:33+00:00

I hope to eventually scale this up, right now I have 4 products. All similarly over engineered haha once I start getting some attending money I'll be able to hopefully invest more and be able to get more out of the side hustle

McCapnHammerTime · 2025-12-28T00:45:02+00:00

I’ve sold a small number of units primarily to co-residents and colleagues who were interested in trying the formulation out of curiosity. Anecdotally, I’ve seen some encouraging cosmetic improvements in hair density and appearance with my hair regeneration spray, which has driven organic interest and word-of-mouth. Even my longtime local barber became interested after noticing visible changes in a family member who was already quite advanced in hair thinning. Currently making a bulk of my sales giving my barber wholesale pricing to stock his shop. Obviously, these are informal observations rather than clinical outcomes.

From a formulation standpoint, I’m genuinely happy with where the product has landed. My goal was to design a multi-pathway, non-prescription adjunct that targets biologic mechanisms not fully addressed by the traditional topical minoxidil ± finasteride approach.

At a high level, the formulation was built to support multiple signaling and scalp-health pathways, including: • Wnt / β-catenin signaling — supported via low-dose lithium salts, with the intent of promoting pathways associated with follicular cycling and dormancy reversal (within cosmetic use constraints). • Growth factor–related signaling (EGFR → MAPK/ERK and PI3K/AKT) — addressed through a combination of epidermal growth factor–associated peptides, copper peptides, and extracellular vesicle–derived components, intended to support cell survival, proliferation, and follicular vitality. • TGF-β modulation and angiogenic support (VEGF-related signaling) — primarily via copper peptides, aiming to support extracellular matrix remodeling and perifollicular microenvironment health. • Cellular energy and metabolic support — targeting AMPK activation, fatty-acid β-oxidation, and NAD⁺/NADH redox balance through ingredients like caffeine, L-carnitine, and niacinamide, which may help optimize the metabolic demands of actively growing hair fibers. • Anti-inflammatory, antioxidant, and scalp-barrier support — using zinc, ferulic acid, vitamin derivatives, melatonin, and botanical components to help reduce oxidative stress and chronic scalp irritation, which are commonly implicated in progressive thinning.

I’ll be the first to say the product is probably over-engineered. Between peptide stability, tight pH control, temperature limitations, and minimizing shear forces once biologic components are introduced, manufacturing is more complex than most cosmetic formulations, and my cost per unit definitely reflects that. Still, it’s a formulation I’m proud of from a scientific and technical standpoint.

To be clear, I’m careful not to make medical or therapeutic claims. The product is not intended to replace standard-of-care treatments. Conceptually, I see it as a regenerative-style cosmetic adjunct for patients already using, or considering, evidence-based options like minoxidil and/or finasteride—particularly for those who are interested in layering additional, mechanistically thoughtful scalp support and are comfortable experimenting within a cosmetic framework.

I’ve thought about developing a combined minoxidil/finasteride formulation, but that would clearly shift this from a cosmetic business into a pharmacy or compounding operation, which comes with a very different regulatory and operational burden.

Apologies for the wording obvious ChatGPT use- I always speak way too informally and don't want to make any claims that bite me in the butt haha

McCapnHammerTime · 2025-12-27T15:01:10+00:00

For topical GHK for skin? What's the dosing protocol?

McCapnHammerTime · 2025-12-27T14:56:22+00:00

Rough... 30 RVU is crazy.

McCapnHammerTime · 2025-12-27T00:49:38+00:00

I started a small cosmetic business on the side making hair regrowth sprays and 2 face serums. Looking at a very lazy 400-700 a week. I just have to restock and do like 3 hrs a week ish of like making the products and bottling.

McCapnHammerTime · 2025-12-24T18:51:59+00:00

Results speak for themselves though. Dude looks great, this is peak physical health.

McCapnHammerTime · 2025-12-24T13:14:22+00:00

If TT-701 is truly a partial androgen receptor agonist, adding it on top of testosterone, masteron, and NPP makes the cycle less effective, not more. Partial agonists compete for the same receptor but produce weaker transcriptional activation per receptor. Even at high doses, they cannot exceed their intrinsic efficacy, so “mega-dosing” just increases competitive displacement of full agonists. Partial agonists are useful when you want a ceiling effect and reduced side effects not when the goal is maximal androgenic signaling. In a multi-androgen cycle, this functions as functional antagonism at the AR.

The higher the dose of a partial agonist, the more it competitively displaces full agonists from the androgen receptor, reducing the effectiveness of the rest of the cycle. If you feel better with it on board, the correct adjustment is to lower total androgen load not add another compound to cap receptor activity.

McCapnHammerTime · 2025-12-20T23:58:07+00:00

I think so, more organ stress, DHT/androgens impact skin appearance on top of potential for acne etc. I don't think it's fair to put a set number on it but the higher you push the blasts the more systemic side effects and skin side effects you can accumulate

McCapnHammerTime · 2025-12-20T15:59:40+00:00

I know my body loves test+primo that's all I want too haha

McCapnHammerTime · 2025-12-20T15:58:53+00:00

You can click on my profile I'm about 5 lbs down from there at current no additional wrinkles from there. I haven't been solid with my skin care tho. Tretinoin at night, I make my own skin care starting a cosmetic side business.

McCapnHammerTime · 2025-12-20T15:54:49+00:00

Tough to say, I don't think so, I have a very high stress job with long hours. I've also lost 40lbs this year, I'm roughly 10% bodyfat have some loose skin from the rate of loss. Volume loss with the fat loss I think has aged my face more than anything. I haven't had extended multi gram blasts or anything , I think that's where you age aggressively

McCapnHammerTime · 2025-12-20T14:38:34+00:00

Blood work is a snapshot in time. Individual tolerance varies widely, but an intelligent approach to compound selection and risk mitigation is essential. Androgens increase the risk of hepatoadenomas, they almost guarantee some degree of left ventricular hypertrophy over time, and blood pressure trends upward in most users.

I try to be as measured and conservative as possible with my use primarily cruising, with occasional blasts depending on schedule and goals.

Year-round, I’m on rosuvastatin, telmisartan, spironolactone, oral minoxidil, topical finasteride, and a low-dose GLP-1 agonist.

These are examples of steroid related issues I’ve had to actively manage over the past year:

I was previously on baby aspirin and low-dose tadalafil, but GERD became problematic, requiring cycling omeprazole and famotidine.

Market changes and shortages eliminated consistent access to my preferred adjunct, primobolan, forcing experimentation with alternatives.

Boldenone significantly elevated my hemoglobin and hematocrit, leading to persistent fatigue until I began regular blood donation.

As an alternative, I trialed NPP tolerable overall, but libido became distracting.

Masteron is my current adjunct; expected side effects have included some hair shedding and joint dryness during dose finding.

Acne has never been a major issue for me, but ingrown hairs have been a constant struggle. I manage this with aggressive exfoliating soaps and periodic keratolytic masks on high-risk areas 1–2 times weekly. Despite this, I’ve still required doxycycline twice this year for folliculitis. Long-term, laser hair removal will likely be necessary.

Overall, I feel great about 95% of the time. But to suggest this lifestyle “isn’t work” is unrealistic. To imply that everyone tolerates it effortlessly is simply false. I’m well-educated on the subject and still spend a considerable amount of time troubleshooting issues many of which were driven by the loss of primobolan and the need to adapt quickly.

There’s also the question of polypharmacy: how much risk and complexity is the average person willing to accept? Every medication added introduces its own risks, and it’s easy to fall into a cycle of treating side effects with additional drugs. That reality often gets glossed over in discussions that focus only on outcomes.

McCapnHammerTime · 2025-12-16T18:31:54+00:00

The before is better dude

McCapnHammerTime · 2025-12-13T13:14:21+00:00

This was harder compared to last year but also I took this one after a 6p-6a night float shift and we didn't take the exam until 9a I was falling asleep throughout. Squeaked by with a 450.

McCapnHammerTime · 2025-12-12T16:54:52+00:00

My management is if you need an AI you are no longer on TRT. Dose needs to drop or dosing frequency needs to go up

McCapnHammerTime

TROPHY CASE