Whose used this? I have some, running 200mg a day, deffo sweat a bit more during cardio, if I combine it with SLU I get a noticeable increase in body temp. Not sure on dosing as see people saying once per day, multiple times etc. Anyone got experiences and share what they have found?

I am one of those people who on day one when I used Metashred (BAM/SLU combo) it sent me to the ER. Tried again a week later and although I was able to stay away from the ER it wasn't a pretty couple of hours. I decided instead to split up the two (SLU on training days and BAM on rest days). Been using SLU for a while at various dosages with no issues. For BAM, the capsules I have are 15mg. Took my first dosage yesterday on my rest day without issue. Is there a dosage I should be working up to?

I was wondering if you have archives of your articles? I just read this article from the SR about VIP and I cannot tell if it is good or bad (after already placing an order). So looking for more clarity about using it.

Thanksgiving has a way of slowing life down just enough for you to actually notice what’s been happening underneath all the noise. You sit with people you love, share a big meal, breathe for the first time in weeks, and suddenly you’re able to feel things you usually ignore. Maybe this year, in that moment of stillness, you noticed something strange: your body feels strong, your training is dialed in, your glucose looks perfect… but your brain doesn’t match how good the rest of you feels. Maybe you felt foggy after a meal, mentally slower than usual, overwhelmed for no reason, or just “not as sharp,” even though everything on paper says you’re metabolically healthy. If that sounds familiar, you are not alone and there’s a real physiological explanation behind it. How can someone be physically insulin-sensitive yet mentally sluggish? How can your muscles get the fuel they need while your brain feels like it’s running on fumes? This article is written for you, to answer exactly that question. Central insulin resistance is the phenomenon where your brain becomes insulin-resistant even when the rest of your body remains highly insulin-sensitive. Many people experience this as a strange mismatch: they feel physically strong, metabolically healthy, and steady during training, yet their cognition feels foggy, slow, unpredictable, overwhelmed, or “under-powered.” This article explains why that happens, what the mechanisms are, how to recognize the patterns, and how to fix them, using simple language without sacrificing the biochemical accuracy that clinicians and experts expect. The first thing to understand is that the brain handles insulin differently from the rest of the body. Your muscles and liver respond directly to insulin in the bloodstream. The brain does not. For insulin to have any effect in the brain, it must cross the blood–brain barrier, bind to receptors on neurons, activate the PI3K-Akt pathway, and allow neurons to take up and use glucose. If anything disrupts that sequence, neurons will be under-fueled even if the entire rest of the body is functioning perfectly. This is why someone can have excellent fasting glucose, low insulin, perfect CGM curves, and still feel terrible cognitively. The brain can become insulin-resistant before the body gives any signal.

Wearable sweat and interstitial fluid lactate sensors sit at a really interesting intersection: they’re trying to listen in on your cellular metabolism in real time, without ever sticking a needle in your vein. To understand what they can and can’t do, we need to zoom all the way down to the level of glycolysis, redox balance, and membrane transport and then zoom back out to how an athlete or clinician can actually use them on a bike, in a clinic, or during rehab. At the molecular level, lactate is not “the bad guy” or a simple waste product. It is the output of glycolysis when pyruvate is reduced to lactate by lactate dehydrogenase (LDH). In that reaction, NADH is oxidized back to NAD+, which is the real bottleneck: you must regenerate NAD+ to keep glycolysis running when ATP demand is high and mitochondrial oxidative phosphorylation is at or near capacity. So lactate is actually part of a redox recycling system. When intensity rises, ATP demand spikes, glycolytic flux accelerates, the cytosolic NADH/NAD+ ratio climbs, and funneling pyruvate to lactate keeps the system from stalling. The lactate can later be oxidized as a fuel in other tissues (heart, oxidative fibers) or sent to the liver for gluconeogenesis (Cori cycle). This means lactate is both a redox valve and a mobile carbon shuttle. The classic “lactate threshold” is really a systems-level signal that glycolytic production of lactate has started to outpace its clearance and oxidation. As work rate increases, you see a relatively flat lactate curve at lower intensities, followed by a first noticeable rise (often aligned with ventilatory threshold) and then a steeper, exponential climb as mitochondrial capacity and clearance mechanisms are saturated. This shift is tightly coupled to changes in the NADH/NAD+ ratio, mitochondrial membrane potential, oxygen delivery, and monocarboxylate transporter (MCT) activity along the sarcolemma and capillary endothelium. MCT1 and MCT4, for example, move lactate (plus a proton) across membranes, shaping how quickly lactate exits working muscle into blood, then into other tissues. So a lactate “curve” is really a visible fingerprint of how your whole electron transport and substrate-handling system is coping with stress.