I remember my first low-carb meal like it was yesterday—a creamy bowl of soup in a diner with my wife’s college friends. I choked it down. Unctuous. So much fat!
[me in a Farmer hat!}
That was December 2007. I had just finished reading Gary Taubes’ Good Calories, Bad Calories and vowed that nary a gram of carbohydrate would ever again cross my lips, so help me God.
Taubes’s book—essentially a 500-page exposé, written like a giant New Yorker article—laid bare the royal shitshow that has passed for nutrition “science” for the past 80 or so years. It convinced me to ditch the foods I once considered healthy: quinoa, cranberry juice, Clif bars. In their place? Steak, butter, leafy greens.
Hooray?
I had never been a carnivore, so the prospect of a lifetime of red meat and blobs of fat wasn’t exactly thrilling. But I follow (correct) science where it leads, and science had spoken.
Fast forward nearly twenty years. I’m still a devout believer in the keto gospel (Exhibit A: this Substack). At almost 49, I’m strong, lean, and crushing my high school erg times on the rowing machine. I still feel like I’m in my mid-30s. I even got carded last year. (Okay, it was at a dimly lit rock concert, and I was wearing a hat to conceal my considerable baldness. But still.)
I can go days without eating, power through 12-hour chess tournaments, and often outlast (much) younger opponents simply because I have more energy.
My n=1 keto experiment should surprise no one paying attention. The evidence for keto as the should-be-treatment-of-first-resort for metabolic disease is overwhelming.
Gaze upon keto’s likely power (via these links) for dealing with epilepsy, migraines, diabetes, Alzheimer’s, Parkinson’s, PCOS, nonalcoholic fatty liver disease, heart disease, cancer —the list goes on.
And, of course, keto seems to work pretty damn well for fat loss. That’s why most people try it. See here, here, and here.
If keto were a pill, it would be worth a trillion dollars and outsell Ozempic 100x over.
And yet… why it works is still debated, particularly when it comes to fat loss.
Two main schools of thought compete:
• Calories In, Calories Out (CICO): The mainstream view says keto works because it makes you eat fewer calories. It suppresses appetite and/or increases energy expenditure, leading to a “negative energy balance.” If you’ve read any of my Substack, you know that I hate this idea with a burning white-hot passion. (One rejoinder—keto ALSO appears to resolve anorexia by making anorexics gain weight “in all the right places.”) For Taubes’s evisceration of CICO, more technical than mine, see here.
• The Carbohydrate Insulin Model (CIM): Eating carbs makes you secrete insulin, the master regulator of fat storage. High insulin locks fat in fat cells. Switch to keto, insulin drops. The “negative stimulus of insulin deficiency” causes fat to be released and burned for fuel. A calorie deficit still happens—it must, per the laws of physics—but it’s incidental. In the words of legendary diabetologist George Cahill, “carbohydrate is driving insulin is driving fat.” (Ironically, Cahill was, I believe, a staunch CICO person until he died.) Detailed explanation of the CIM is here.
Unsurprisingly, I’m a CIM believer. I’d bet my life (and, in fact, I have!) that keeping insulin low is the key to fat regulation and general good health.
However, the CIM is complicated. A too-simple reading can lead you astray:
• Carbs aren’t the only thing that affects insulin. Protein stimulates insulin, too, albeit to a lesser degree.
• Different foods impact insulin differently for different people at different life stages.
• Cutting carbs may help you lose 50 pounds, but the last stubborn 15 might not melt away so easily on steak and broccoli.
• Entire cultures—Okinawans, Kitavans—eat carbs with abandon and never develop obesity or metabolic disease.
• And what about the star McDougalers? Devoted high-carb vegans who somehow get healthier eating the opposite of how I and Taubes do…
• Even stranger, look at the Kempner rice diet experiments—pure carbs, yet seemingly effective for some. WEIRD.
• Also, insulin—while the 800-pound gorilla of fat regulation—isn’t the only hormone involved. Growth hormone, testosterone, prolactin, enzymes like lipoprotein lipase, and an alphabet soup of other factors all have a say.
• To wit, fat gain and loss can happen outside the insulin-carb paradigm. A favorite example: fat gain that happens when you quit smoking. Here’s the gist. Nicotine suppresses lipoprotein lipase (LPL) a key fat-storage enzyme. When you quit -> nicotine levels drop -> LPL activity increases -> fat storage increases. This has nothing to do with carbs, insulin, or excess calories. (In Gary Taubes’ more precise language, from GCBC: “nicotine induces weight loss by working on fat cells to increase their insulin resistance, while also decreasing the lipoprotein-lipase activity on these cells, both of which serve to inhibit the accumulation of fat and promote its mobilization over storage.”)
I’m not saying this to throw the CIM under the bus. If the world embraced even the most Neanderthal-like interpretation of CIM—carbs bad, make too much insulin, ooga booga!—we’d still cure obesity and most diseases of civilization in months.
That said, we can do better. And the Farmer Model can help us.
Let’s dive in. I’ll illustrate with three examples from my own experiences.
Exhibit A: Vyvanse Rebound Weight Gain
[an actual picture of me on Vyvanse]
Twelve years ago, I was briefly prescribed Vyvanse—a mild stimulant like Adderall—to help with (purported) mild ADHD. It wasn’t a high dose, but I loved the effects. When I took it, I felt locked in and hyper-focused. Not a huge surprise, since it’s basically meth. And who doesn’t love meth?
Eventually, I decided that taking this substance probably wasn’t in my best long-term interests, and I quit.
Within a few weeks, I noticed my weight uncomfortably drifting upwards. I gained 6-7 pounds without changing anything (that I could consciously detect) about the diet/lifestyle that had kept me weight-stable for years. What was going on? Could quitting the ADHD meds have played a role?
The CICOs would argue, naturally, that quitting stimulated my appetite and made me eat more than I had been eating. Likely story.
A too-narrow reading of the CIM might say that quitting Vyvanse made me sneak in extra carbs and/or perhaps the medicine had been altering insulin levels. Definitely not with the carbs, maybe with insulin.
Well, as the saying goes, it was time for me to “do my own research.”
Turns out, weight rebound after quitting stimulant meds is well-documented. The literature overfloweth.
• Random paper (“withdrawal from drugs of abuse is associated with overeating and weight gain.”)
• Random Reddit thread on post-Vyvanse weight gain. Read the comments—wild.
• Another study showing that kids who quit ADHD meds experience rebound weight and height growth.
Based on these types of accounts, I came to the conclusion that the best course of action was just to do NOTHING. Allow the system to reset over the course of 10-12 months. The weight should go away, and I’d return to my previous “better” weight.
So I did that. And that’s EXACTLY what happened.
No monkeying with diet or exercise needed. Just time for homeostasis to restore itself.
The Farmer Model Explanation—Hidden Pipes
Keto (among other things) had been powering my metabolic farm just fine—water levels steady, irrigation dialed in, crops thriving just as they should. Then I took Vyvanse, and without me realizing it, the land itself subtly changed. It was like installing hidden drainage pipes beneath the soil, quietly siphoning off water so the fields stayed drier than they otherwise would be.
Then one day, I yanked out the pipes.
Suddenly, water that had been draining away had nowhere to go. It pooled in places that had been drier for months. The soil, unaccustomed to the sudden influx, got boggy. Crops swelled. I “gained fat”—not because I was overeating, and definitely not because my metabolism had broken, but because the farm was adjusting to the abrupt shift in drainage patterns.
But land is resilient. The excess water didn’t stay forever. Bit by bit, the soil absorbed what it needed, the rest evaporated, and my farm found its natural balance again—no intervention required. Just time.
Exhibit B: Couvade’s Syndrome Weight Gain
[My wife’s pregancies changed me—a LOT]
Another curious experience.
We have three kids. Every time my wife got pregnant, I gained 7-8 pounds like clockwork during the third trimester—weight that stuck around for several months after the babies were born, and then just as mysteriously vanished as they exited babyhood.
Once again, I changed absolutely nothing (to my conscious knowledge) about my keto diet or lifestyle during these fluctuations. I wasn’t tracking every calorie or gram of carb, so who knows? But I wasn’t stress-eating pints of ice cream either.
This phenomenon—expectant fathers gaining weight and experiencing other metabolic shifts—is well-documented and known technically as Couvade’s Syndrome. It’s perfectly normal. Google’s AI confidently reports that it happens to somewhere between 11% and 65% of dads. (Thanks for that precision, Skynet.) Meanwhile, this 2007 review claims it impacts 97% (!) of fathers. Whatever. It’s a thing.
The CICOs, as is their wont, blame the weight gain that accompanies Couvade’s on overeating. It’s a psychological phenomenon, they say. Stress, sympathy eating, subconscious insecurity about impending fatherhood. ETC!
Then again, tamarins and marmosets—small primates that also exhibit paternal care—get Couvade’s, too. Riddle me this: how exactly do tamarins and marmosets experience “pseudo-sibling rivalry, identification with the fetus, ambivalence about fatherhood, a statement of paternity, or parturition envy”? Hmm?
Stupid, stupid, stupid. CICO is a trash theory for explaining metabolic reality.
Anyway! Let’s turn to CIM. Could this be specifically related to carbs/insulin? Unlikely. Right?
Other hormones also have a say in how, when, and why we fatten. Sure enough, research finds that men experience higher concentrations of prolactin and cortisol in the period just before birth and lower postnatal concentrations of sex steroids. Key idea here: “This pattern of hormonal change in men and other paternal mammals, and its absence in nonpaternal species, suggests that hormones may play a role in priming males to provide care for young.”
Hormonal adaptation, not overeating. Couvade’s messes with the homeostasis governing fat regulation. Forget calories, forget carbs, forget insulin, forget Freud and pals.
QED. Mystery solved. I’ll take my Nobel Prize, please.
The Farmer Model Explanation: The Seasonality of Fatherhood
For most of human history, pregnancy and childbirth weren’t just personal milestones—they were survival events. Infants were fragile. Maternal mortality was high. New fathers weren’t out there posting nursery photos—they were in survival mode.
So, the body does what any well-run farm does before a rough season: it prepares.
• Prolactin rises, testosterone dips → This isn’t just a random shift; it’s surely an adaptative repsonse. Lower testosterone makes dads less aggressive, more nurturing, and more bonded to their newborns. It’s like the farm sensing an incoming wet season—more moisture retention, less runoff.
• Cortisol increases → The ancient father wasn’t chilling in a hospital room; he was on high alert, scanning for threats. That’s cortisol doing its job—signaling the body to store energy because unpredictable times are ahead.
• Fat storage ramps up → A father carrying a little extra weight isn’t a fluke—it’s an evolutionary safeguard. What if food becomes scarce? What if the mother can’t forage or hunt because she’s recovering? What if the father suddenly needs to survive on stored energy while keeping a newborn alive? The farm doesn’t just produce crops in times of abundance; it lays down extra reserves in case of famine.
Then, the baby arrives.
• Postpartum hormone shifts trigger another transition. The “fatherhood season” recedes. The body, sensing the immediate survival pressures have eased, releases the stored energy. The land dries, the terrain rebalances, and just like that, the extra weight vanishes without intervention—the same way fields return to their usual rhythms after a rainy season ends.
This is why CICO and CIM fail to explain Couvade’s Syndrome. It’s not about overeating. It’s not about insulin, per se. It’s about adaptation. Your body, like the farm, isn’t malfunctioning—it’s responding to the season it’s in.
And this is true of more than just fatherhood. Fat gain isn’t always pathology. Sometimes, it’s just the metabolic equivalent of a rainy season.
Exhibit C: Weight Gain from Too Many Heavy Cream Lattes
[Yum.]
I’ll keep this short because this post is already almost a book unto itself.
Long story short, about four years ago, for reasons that have been lost to time, I started drinking more and more heavy cream lattes. Like 2-3 per day. I figured that heavy cream has virtually no carbs, so why not go to town?
Well, you know where this is going. I gained another 7-8 pounds, and this time, I couldn’t blame the rebound on Vyvanse or my children. After some introspection, I came to suspect the heavy cream lattes might be to blame.
I’m not going to play the game of pinpointing the exact culprit—maybe the dairy was stimulating insulin in an unexpected way, or maybe even the excess coffee itself was triggering a hormonal response. I vaguely recall reading theories about both, but frankly, I’m too lazy to go spelunking through PubMed to find relevant links.
Anyway, the CICOs would say, Duh, excess calories!—as if that alone explains why weight gain happens. (Yawn. Wrong. Moving on.) The CIM crowd would argue that something in those lattes—whether the dairy proteins or even the coffee itself—was stimulating insulin in a way that wasn’t obvious just from looking at the carb count. That explanation, to me, seems far more likely.
Bottom line: I cut the lattes, and my weight fell right back to baseline.
The Farmer Model Explanation: A Hidden Shift in the Terrain
Not all metabolic disruptions look the same—some are obvious (like sugar), while others sneak in under the radar (like heavy cream). This is where the Farmer Model gets interesting: different things reshape the metabolic landscape in different ways. Not all shifts are seasonal (like Couvade’s Syndrome), and not all damage comes from an obvious source (like high-carb diets). Sometimes, the terrain changes in ways you don’t expect.
Again, try to think of your metabolism like farmland. The most obvious disruptor might be (say) “acid rain”—high-carb, sweet, ultra-processed foods that erode the topsoil, flood the land, and cause obvious metabolic damage (fat storage, inflammation, insulin spikes). But not all disruptions look like a storm.
In this case, maybe the lattes weren’t a deluge of acid rain; they were something more insidious—like nutrient imbalances in the soil. Maybe the dairy proteins stimulated insulin in a subtle but persistent way. Maybe they altered gut signaling in the wrong direction. Maybe it was like adding too much fertilizer to a field—not immediately catastrophic, but over time, the land stops functioning the way it should.
Various forces—not just carbs or calories—can shift the topography of your farm. Some changes are temporary and self-correcting (like Couvade’s). Others, if left unchecked (like those damn lattes), could lead to longer-term metabolic dysfunction.
What’s Your Point with All This, Adam?
1 Not all fat shifts are bad. Fluctuations in body fat can be pathological or non-pathological (I mean, right?), and it’s hard to tell which is which just by measuring the total water (fat) on the farm or even looking at the changing landscape. Sometimes, fat gain is expected and temporary (Couvade’s Syndrome—a season of life). Sometimes, it’s actually part of a healing process (getting off ADHD meds and restoring homeostasis). Sometimes, it’s a clear metabolic red flag (the heavy cream latte situation). Context matters. Don’t assume all weight gain means something is broken.
2 Sometimes the answer is simple. The 80/20 rule of fat loss and maintenance may well be “keep insulin low by keeping carbs low”—no need to overcomplicate it. But sometimes, the body is a black box of weirdness and almost impossible to fully decode.
3 Beware gurus with “one-size-fits-all” answers. Each situation is individual, and your metabolic farm has its own terrain, weather patterns, and hidden variables.
4 It’s NEVER CICO. Stop thinking about weight loss as calories in, calories out. Think topographically. What’s changing in the landscape? What’s shaping the terrain? THAT’S where the answers have to be.
5 We need more research. But let’s be real—we’re never going to get it. Too much of nutrition science is driven by lazy assumptions, bad funding incentives, and a refusal to abandon broken models. So, we self-experiment and guess and cross out fingers.
What do you think? Have you ever experienced weird, unexplained weight fluctuations on keto?
If so, what do you think caused them? (NO CICO ANSWERS, PLEASE!)
This is a refreshing take on the challenges of the keto diet. It’s so easy to assume that a specific diet will always work, but your experience highlights how important it is to listen to our bodies and adjust accordingly. Great insights!
Great analysis. The big question is, what do you consider “weight gain.” How many pairs of visible abs, if any, is ideal for proper health? Is it better to have an extra five or ten pounds hiding your four or six-pack?
I have a hunch that unwanted weight gain can be an immune response, since fat cells tend to sequester toxins. Lipogenesis could be seen as a form of inflammation.
It’s interesting that you didn’t mention PUFAs at all.
Thanks!