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I knew this 30 years ago, if you are not overweight do mot eat like an overweight person eventually you will become overweight and losing muscle will lead to premature death

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The Smartest Coach in the Room
Every Saturday, The Smartest Coach in the Room delivers helpful takeaways on the hottest nutrition and health topics and the world’s most effective coaching techniques.

The 5-Second Skim: Why Eating More Might Help You Lose Weight

Recognize that ultra-low calorie diets can produce rapid weight loss, but often trigger intense hunger, cravings, and food preoccupation.
Understand that extreme restriction is difficult to sustain, leading many people to unconsciously compensate by overeating at other times.
Consider a more moderate calorie deficit, paired with adequate protein and minimally processed foods, to improve consistency and long-term results.

Are ultra-low calorie diets safe? (Or even effective?)


In general, an “ultra-low” calorie diet is one that has about half the amount of calories it takes for you to maintain your weight.

(For most women that’s around 1200 Calories, and for men it’s around 1500 Calories.)

Ultra-low calorie diets are pretty much guaranteed to cause weight loss, even for those with thyroid problems, and even when you take into account adaptive thermogenesis—or the “slowing” of metabolism after an extended period of caloric deficit.

Problem: Semi-starvation is brutal.

An undressed salad and you’re smiling? Lies.

About 80 years ago, researchers at the University of Minnesota published a study called “The Minnesota Starvation Experiment.”

In the study, 36 men voluntarily semi-starved themselves by eating about half their normal intake. After six months, every single one of them had lost about 25 percent of their weight—no exceptions.

However, they’d also gained something:

An outright obsession with food.

Food preoccupation became so intense for the Minnesota men that they would routinely lick their plates, and even rummage through the trash for scraps between meals.

Biology FTW

When people try an ultra low-calorie diet, they may get results at first, but over time—as the Minnesota study showed—biology makes it harder and harder to sustain.

If you or a client has ever tried to follow an extreme diet for more than a few weeks, you might notice you’ll start to “sneak” in calories—sometimes without even being conscious of it.

Then, of course, progress stalls.

Clients may think they’re still following, say, a 1200 or 1500 Calorie diet, but more likely they’re nailing their calorie targets some days, and wildly exceeding it on others.

“Clients say ‘I’m eating 1200 or 1300 Calories a day.’ That’s usually true-ish. It’s just not consistent,” says Brian St. Pierre, MS, RD, Precision Nutrition’s Director of Nutrition. “They’re in the ballpark four to five days a week, but they’re likely compensating with higher calorie foods on other days.”

Solution: Eat a little more.

If your clients aren’t losing weight despite being on an ultra-low calorie diet, it might actually be that the calorie deficit is too extreme.

So, the counterintuitive solution to stalled or no weight loss on an ultra-low calorie diet is actually to… increase your caloric intake.

By adding just a few hundred daily calories, you’ll reduce the intense hunger, cravings, fatigue, and food obsessions that make it so difficult to remain consistent.

“It feels as if you’re eating more because, on most days, you are,” says St. Pierre. “Yet, while you’ll eat more each day, you’ll likely consume less each week.”

Eating lean protein (at least 4-5 palm-sized portions daily) and focusing on minimally-processed foods, which are more satiating, can also help people eat a little less, feel satisfied, and—often ignored in dieting—maintain precious muscle mass.

Losing weight should feel tolerably sucky.

If someone’s priority is weight loss, a certain amount of hunger is inevitable.

However, if that hunger is so extreme that it’s starting to disrupt someone’s focus, energy levels, or psychological well-being, scale back.

Moderate approaches are almost always more sustainable—and, as a result, lead to better long-term outcomes.

For more wild and kooky ways your biology fights back against ultra-low calorie diets—and what to do about it—read: Is a 1200-Calorie diet (or any super low-calorie diet) actually realistic?



Take care,



Alex Picot-Annand, PN2, Holistic

Nutrition Certification, Coaching & Courses | Precision Nutrition Precision Nutrition is the home of the world's top nutrition coaches. Best-in-class nutrition coaching, nutrition software, and professional certification.

The success of Adaptation
Adaptation generally refers to the process or result of changing to better suit a new environment, condition, or purpose. Its meaning spans several specific fields:1. Biology and EvolutionIn evolutionary biology, an adaptation is any heritable physical or behavioral trait that helps an organism survive and reproduce in its environment. These traits are shaped by natural selection over generations.Structural: Physical features, such as the thick blubber of a polar bear or the water-storing stems of a cactus.Behavioral: Innate actions, such as bird migration or seasonal hibernation.

Eat for life food is medicine
The question is , are Cancer cells a mutation or an adaptation
The answer is yes , that they are a mutation
Tumor Suppressor Genes: Mutated genes that stop working properly, failing to put the "brakes" on cell division or repair DNA damage.Understanding the exact mutations in a tumor allows doctors to use genomic profiling to find specific, targeted therapies. You can learn more about how DNA changes cause this disease through the National Cancer Institute or the Canadian Cancer Society.If you are researching a specific type of cancer or want to know more about testing and treatment options based on these mutations, let me know how I can help narrow down the information!How does cancer start?Cancer starts with changes in the genes of a cell or a small group of cells. These changes cause cells to grow and multiply too much, forming a tumor. **Cell ch...

The Question is are Cancer cells an adaptation or Mutation

Yes !!! Cancer cells are a Mutation Tumor Suppressor Genes: Mutated genes that stop working properly, failing to put the "brakes" on cell division or repair DNA damage.Understanding the exact mutations in a tumor allows doctors to use genomic profiling to find specific, targeted therapies. You can learn more about how DNA changes cause this disease through the National Cancer Institute or the Canadian Cancer Society.If you are researching a specific type of cancer or want to know more about testing !How does cancer start?Cancer starts with changes in the genes of a cell or a small group of cells. These changes cause cells to grow and multiply too much, forming a tumor. **Cell ch...

Dinner the essentials

If you ever wondered who came first, the scientific answer will surprise you If we look back billions of years, the very first life forms on Earth reproduced without males. They did this by cloning themselves. However, science does not classify these ancient, single-celled organisms as "female" or "women." To have a female, a species must also have a male. Instead, these original organisms were simply asexual.2. Males and Females Evolved SimultaneouslyAround 1.5 to 2 billion years ago, long before the first animals, some single-celled organisms evolved a new strategy: instead of cloning themselves, two cells fused their DNA together. This was the origin of sexual reproduction.Eventually, this split into two distinct roles:The "Female" role: Producing a large, nutrient-rich cell (the egg) to feed the potential offspring.The "Male" role: Producing a small, highly mobile cell (the s***m) designed strictly to travel and deliver DNA.Because these two roles evolved together as a cooperative reproductive strategy, males and females emerged at the exact same time in our evolutionary tree. By the time the very first human (Homo sapiens) evolved 300,000 years ago, our ancestors had already been strictly male-and-female for hundreds of millions of years.3. Why Can't Human Women Reproduce Alone?While some modern animals—like certain sharks, lizards, and birds—can successfully trigger parthenogenesis to give birth without a male, mammals cannot.Human reproduction requires a strict genetic lock called genomic imprinting. In humans, certain essential survival genes in the embryo are chemically "turned off" in the mother's egg and can only be activated by instructions found inside the father's s***m (and vice versa). Without a contribution from both a biological mother and a biological father, a human embryo cannot develop normally.If an unfertilized human egg accidentally tries to divide and grow on its own, the lack of paternal DNA causes the process to fail, typically resulting in a disorganized mass of cells called an ovarian teratoma rather than a viable baby.

Build-UPS and break-downs: metabolism impacts on proteostasis ...
Proteostasis and proteome stability. Proteostasis represents ...
Proteostasis (a portmanteau of protein and homeostasis) is the biological process by which cells maintain a dynamic balance of functional, correctly folded proteins both within and outside the cell. According to Wikipedia, it ensures that the cellular proteome (the entire set of proteins) functions correctly under changing environmental conditions and metabolic stresses.

The Core Pathways (The Proteostasis Network)
To achieve this equilibrium, the cell relies on an integrated quality control infrastructure known as the Proteostasis Network (PN). This network actively manages the four major stages of a protein's lifecycle:


Biogenesis (Synthesis): Ribosomes build proteins by translating genetic codes into long amino acid chains.
Conformational Folding: Molecular chaperones assist these nascent chains to fold into unique three-dimensional shapes required for biological function, preventing premature aggregation.
Trafficking: The network carefully directs the finalized proteins to specific target locations inside or outside the cell.
Degradation: Damaged, misfolded, or obsolete proteins are cleared out. This relies heavily on the Ubiquitin-Proteasome System (UPS) for individual targeted proteins and Autophagy-Lysosomal pathways for clearing out larger bulk protein aggregates.

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Why Proteostasis Matters
When cells age or face environmental stresses, the proteostasis network can become overwhelmed or decline. A loss of proteostasis results in the accumulation of misfolded proteins that stick together and form toxic aggregates.

As detailed in research published via PubMed and the National Center for Biotechnology Information (NCBI), a permanent breakdown in this system is a central feature of aging and drives many human diseases, including:
Neurodegenerative disorders: Alzheimer’s disease, Parkinson’s disease, and Amyotrophic Lateral Sclerosis (ALS).
Metabolic and chronic illnesses: Type 2 diabetes and certain forms of cardiovascular disease.
Cancer: Malignant cells often hijack and manipulate proteostasis networks to survive severe cellular stress and rapidly multiply
Now we look at how therapeutic interventions are targeting proteostasis to treat neurodegenerative diseases?

Therapeutic interventions targeting proteostasis seek to prevent, slow, or reverse neurodegenerative diseases by restoring the balance of protein folding and accelerating the clearance of toxic aggregates. Rather than just masking symptoms, these emerging therapies fix the cell's internal quality control systems.


The primary clinical strategies and cutting-edge drug discovery approaches targeting this network include:
1. Upregulating Molecular Chaperones
Chaperones are the cell's frontline defense against misfolding. Boosting them keeps proteins properly folded and functional.


HSF1 Activation: Heat Shock Factor 1 (HSF1) is the master regulator transcription factor for chaperones. Drug candidates like Riluzole modulate HSF1 to upregulate chaperone production, helping cells mitigate neurotoxic stress.
HSP40 Boosters: Small molecules are engineered to upregulate specific Heat Shock Proteins (like DNAJB2 and DNAJB6). These proteins bind to and neutralize the early stages of toxic amyloid-beta (Alzheimer's) and alpha-synuclein (Parkinson's) aggregates.


2. Targeted Protein Degradation (TPD)
If a protein has already misfolded into a toxic clump, the cell must destroy it. TPD utilizes the cell's native disposal system to destroy specific disease-causing targets.

Clarivate
PROTACs (Proteolysis-Targeting Chimeras): PROTACs are multi-functional small molecules that act as molecular matchmakers. They tether a toxic protein (such as mutated tau or TDP-43 in ALS) directly to an E3 ubiquitin ligase, flagging the bad protein for instant destruction by the proteasome. The scientific validation of this mechanism was cemented by the FDA's landmark approval of Vepdegestrant (Veppanu), proving that the cellular disposal line can be successfully engineered for human medicine.
Molecular Glues: These small molecules modify the surface of an E3 ligase so it naturally grabs and degrades "undruggable" disease-driving proteins.

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3. Enhancing Autophagy (Cellular Self-Eating)
When large, complex protein fibrils block the narrow proteasome pathway, the cell must use autophagy to safely wrap aggregates in membranes and melt them inside lysosomes.

National Institutes of Health (.gov)
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mTOR Inhibitors & Beyond: Chemical compounds like Resveratrol or Bosutinib stimulate macroautophagy. This clears out bulky cellular trash and preserves synaptic health.
Signaling Modulators: Recent breakthroughs from institutions like the Hebrew University of Jerusalem have proven that blocking specific cellular complexes (such as certain nucleolar structures) downregulates TGF-β signaling, drastically boosting the cell's natural ability to degrade Alzheimer’s-causing plaques.

Frontiers
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Summary of Therapeutic Classes
Intervention Type Primary Mechanism Disease Targets Status / Example
Proteostasis Regulators Restores the baseline balance between protein synthesis and breakdown. Cystic Fibrosis, Huntington's CFTR Correctors (Clinically approved for CF)
PROTACs & Glues Forcibly tags disease-causing proteins for proteasome destruction. Alzheimer's (Tau), ALS (TDP-43), Cancers Vepdegestrant (First FDA approved PROTAC)
Autophagy Inducers Triggers bulk lysosomal clearing of large, toxic protein aggregates. Parkinson’s, Alzheimer’s, Dementia Bosutinib, Resveratrol (Under Active Research)
4. Lifestyle-Driven Proteostasis Activation
Clinical drugs are not the only way to regulate this pathway. Robust epidemiological and clinical data published on PubMed Central (PMC) highlights that specific lifestyle choices act as natural proteostasis activators:

Key Points

Physical Exercise: Sustained physical activity releases myokines (like irisin), which cross the blood-brain barrier to directly activate autophagy degradation, reversing age-related proteostasis decline.
Caloric Restriction / Fasting: Depriving the body of constant nutrient streams directly triggers the cell to scavenge and digest its own internal damaged protein aggregates for fuel.

Now take a closer look at a specific disease, such as how PROTACs target TDP-43 in ALS, or should we look at the specific dietary and lifestyle interventions that optimize
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This is for informational purposes only. For medical advice or diagnosis, consult a professional. .

Dieting is not about restrictions
It is about moderation and better food choices