Tag: health

Is Yo-Yo Dieting Bad for You? Weight Cycling Explained

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

A lot of my patients describe the same arc. They work hard, lose weight, feel good for a while, and then months or years later it comes back. That repeated loss and regain is weight cycling. It is common, and it is hard on people both physically and emotionally.

The question I hear most often is whether it is even worth trying if the weight is coming back anyway. The research answers that more clearly than it used to, and the answer is yes.

Weight cycling generally means repeated intentional loss followed by unintentional regain. Some researchers set the bar at a 10 percent change in body weight occurring three or more times. Depending on the study, it affects 20 to 35 percent of men and up to half of women (Montani et al., 2015).

Why does the weight return? Biology pushes back harder than most people anticipate. After weight loss, resting energy expenditure falls further than body size alone would predict, and this metabolic adaptation can persist for years, meaning the body burns less than expected (Fothergill et al., 2016). Hormones move too. Leptin drops, hunger hormones climb, and patients end up hungrier and less satisfied by meals than they were before (Sumithran et al., 2011). The body also tends to compensate for exercise by raising appetite. Together these explain why maintenance is the hard part, not the losing (Thomas et al., 2012).

The real question is whether the cycling itself does damage. Large reviews and cohort studies have not found strong evidence that weight cycling raises mortality or major chronic disease risk when the weight loss is intentional and supervised (Mehta et al., 2014). Some work suggests regain may favor fat over muscle, visceral fat especially, though the findings are inconsistent (Mackie et al., 2017).

The psychological picture is better than most people assume. Foster and colleagues found that patients who regained weight still reported improvements in mood, hunger, and eating behavior after the loss phase (Foster et al., 1996). Other work has found no consistent long-term harm from the pattern itself (Osborn et al., 2011).

So should patients keep trying? The National Task Force on the Prevention and Treatment of Obesity concluded in 1994 that weight cycling should not deter people from attempting weight loss, and that position has held up (National Task Force, JAMA 1994). The benefits of intentional loss, lower blood pressure, better lipids, better glucose control, better quality of life, generally outweigh the risk of regaining.

One of my patients lost about 8 percent of her body weight through diet and walking. A year later most of it had come back. During the stretch she kept it off, though, her blood pressure normalized and she came off one of her antihypertensives. The weight returned. The benefit she got during that window was real and measurable, and the research says her experience is the rule rather than the exception.

What I steer patients toward is sustainable habit rather than another aggressive diet. Regular activity, consistent eating patterns, decent sleep, and watching the trend line instead of the daily number. A setback does not undo the progress. Staying connected to support, whether that is a clinician, a dietitian, or counseling, matters more than most people expect.

Weight cycling is real and it is discouraging. It is not a reason to stop. Even temporary weight loss buys real health, and the useful reframe is to treat weight management as ongoing care rather than a project with an end date.

Scott Rennie, D.O.

References

Montani JP et al. Obesity Reviews. 2015.

Fothergill E et al. Obesity. 2016.

Sumithran P et al. NEJM. 2011.

Thomas DM et al. Obesity. 2012.

Mehta T et al. Obesity Reviews. 2014.

Mackie GM et al. Obes Res Clin Pract. 2017.

Foster GD et al. J Consult Clin Psychol. 1996.

Osborn CY et al. Ethn Dis. 2011.

National Task Force on the Prevention and Treatment of Obesity. Weight cycling. JAMA. 1994;272(15):1196-1202.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

How Much Exercise Do You Need to Lose Weight?

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Patients ask me all the time how much exercise really matters for weight loss. The honest answer is that it depends on what they are trying to do. Losing weight quickly, keeping it off, and staying healthy are three different goals, and exercise performs very differently against each one.

On one point the research is not ambiguous. Exercise on its own rarely produces large weight loss. Most trials show modest changes, roughly half a kilogram to three kilograms, and that is in people putting in 180 to 270 minutes a week (Jakicic et al., 2019). Below 150 minutes, most people do not lose much at all. I see the same thing on my schedule. Patients who start walking three times a week often feel noticeably better while the scale barely moves, and that gap is worth naming out loud before they get discouraged by it.

None of which makes exercise optional. It is among the best tools we have for preventing regain. Long-term data show that people sustaining higher volumes, often north of 250 minutes a week, are considerably more likely to hold onto a 10 percent loss (Jakicic et al., 2014). That is where the real return sits.

Paired with dietary change, the numbers improve. Adding exercise to calorie restriction increases short-term loss by about 20 to 25 percent over diet alone (Wing et al., 1998; Goodpaster et al., 2010). I had a patient who was cutting calories carefully and getting almost nothing for it until she added regular cycling. With both together she lost roughly twice as much and held it considerably longer.

Type and volume both matter. For general health, 150 minutes of moderate activity a week is the baseline. For meaningful weight loss, 250 to 300 minutes is closer to what is needed. For maintenance, somewhere in the 200 to 300 range seems to work. None of this requires a gym. Walking, yard work, and even light activity like standing or slow walking accumulate, and a 2021 doctoral dissertation found that increasing light-intensity activity independently predicted weight loss at both 6 and 12 months (Jackson, 2021).

Practically, I tell patients to start from where they actually are. Adding steps, breaking up long stretches of sitting, and picking something they do not dread produces more consistency than any prescribed routine they will abandon in a month. Thirty to sixty minutes on most days works whether it comes in one block or four. And if weight loss is the goal, it has to be paired with dietary change; exercise alone will disappoint them.

Exercise is not a shortcut to weight loss, and patients who come in expecting it to be will be let down. What it does do is keep lost weight off, improve metabolic health, and protect function as people age. Move more, sit less, keep going.

Scott Rennie, D.O.

References

Jakicic JM et al. Physical Activity and the Prevention of Weight Gain in Adults: A Systematic Review. Med Sci Sports Exerc. 2019;51(6):1262-1269.

Jakicic JM et al. Obesity. 2014;22:2284-2292.

Goodpaster BH et al. JAMA. 2010;304(16):1795-1802.

Wing RR et al. Am J Clin Nutr. 1998;67(3):551-558.

Physical Activity Guidelines Advisory Committee. 2018 Scientific Report.

Jackson R. Doctoral dissertation, 2021.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Does Fasting Slow Aging? What the Science Says

On By Dr. Scott RennieIn Longevity & Healthy AgingLeave a comment

Aging cannot be stopped. The pace of it may be influenced by what and when we eat, and that idea is old rather than new. Since the 1930s, animal studies have shown that cutting calories without causing malnutrition extends lifespan. Rodents held at a 30 percent reduction lived longer with less cancer and less heart disease.

The proposed mechanisms are lower oxidative stress, better mitochondrial function, and less inflammation. Less fuel in, less metabolic wear.

Then you move from mice to people and it gets complicated.

The CALERIE trials brought calorie restriction into human research. CALERIE II found that cutting roughly 15 percent of calories for two years improved blood pressure, cholesterol, and markers of oxidative stress, and those benefits appeared without major weight loss (Kraus et al., 2019). The obstacle is adherence. Sustained restriction is hard on mood, on social life, and on nutritional balance, and most people will not hold it.

Which is how fasting patterns entered the conversation. Intermittent fasting covers several approaches. Some people fast on alternate days. Others follow 5:2, eating normally five days a week and restricting on two. Time-restricted feeding, which confines eating to an 8 to 10 hour window, has drawn the most recent attention.

Alternate-day fasting does produce fat and weight loss, but hunger is a serious barrier and dropout rates run high. Modified versions have not clearly outperformed standard calorie restriction (Trepanowski et al., 2017).

Time-restricted feeding looks more workable. Sutton and colleagues tested an early schedule with all meals between 7 a.m. and 3 p.m. Participants did not lose weight, but insulin sensitivity, blood pressure, and oxidative stress markers all improved, and they reported less hunger through the evening (Sutton et al., 2018). Other short-term work points the same direction, particularly on appetite control and metabolic flexibility (Hatori et al., 2012; Varady et al., 2022).

What does that mean in practice? Calorie restriction has the strongest animal data and some genuinely promising human results, and almost nobody sustains it. Alternate-day fasting rarely survives contact with real life. Time-restricted feeding is the one most patients can actually keep, and even moving to a 10 hour window and dropping late-night meals is a defensible starting point.

When I talk this through with patients, I usually suggest starting at a 12 hour window and tightening it only if they tolerate the change well. What goes in the window still matters more than the window does, and nutrient density should not get lost in the enthusiasm about timing.

Fasting is one tool among several, and which one fits depends on the person, their health, and what they can hold onto for longer than a month.

Scott Rennie, D.O.

References

Ravussin E, Redman LM et al. 2015.

Kraus WE et al. Lancet Diabetes Endocrinol. 2019.

Sutton EF et al. Cell Metab. 2018.

Trepanowski JF et al. JAMA Intern Med. 2017.

Heilbronn LK et al. 2005.

Spadaro PA et al. 2022.

Hatori M et al. Cell Metab. 2012.

Varady KA et al. 2022.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Do Weight Loss Supplements Work? What Research Shows

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Patients ask me about supplements constantly. They have seen an ad promising fast results from something natural and want to know whether it is worth a try. The answer is duller than the advertising. The evidence behind most weight loss supplements is thin, and the safety problems are not.

Paul R. Thomas at Columbia University’s Institute of Human Nutrition has reviewed this literature. What he and others find is that these products mostly do not work. The studies that exist tend to be small, short, and funded by the companies selling the product. Where a benefit shows up, it is small. Garcinia cambogia came in at under a kilogram of difference against placebo. That is not what patients are hoping for when they buy it, and it is not remotely close to what lifestyle change or an FDA-approved medication will do (Thomas, 2022).

The marketing claims sort into a few categories. Appetite suppression is credited to hoodia, glucomannan, and saffron. Metabolic or energy boosting gets attributed to caffeine, green tea extract, and bitter orange. Fat absorption blocking is the pitch for chitosan, and reduced fat synthesis for CLA and garcinia cambogia. The proposed mechanisms sound reasonable. The measured effects are close to nothing.

Safety is the more serious issue. Supplements do not have to be proven safe or effective before they are sold, because they are regulated closer to food than to drugs. The FDA can generally act only after harm is documented, which leaves a wide window. Independent testing has repeatedly turned up quality failures, including heavy metal contamination and doses that do not match the label. Some products have been found to contain banned or genuinely dangerous drugs, among them sibutramine, pulled from the market over cardiovascular risk, and phenolphthalein, a carcinogen (Tucker et al., 2018).

The harm is documented rather than theoretical. Roughly 23,000 emergency department visits a year in the United States are attributed to supplements, and weight loss and energy products account for most of them. The usual presentations are palpitations, chest pain, and tachycardia, and the patients are disproportionately young adults in their twenties and early thirties (Geller et al., 2015).

When patients ask what to do, I tell them to be careful. If they are going to use something, single-ingredient products from established national brands are the safer end of the pool, ideally with third-party verification such as USP or NSF. Avoid proprietary blends that will not disclose what is in them. Be suspicious of anything promising to melt fat. If they have a reaction, stop the product, keep the bottle, and report it to Poison Control and the FDA’s MedWatch program.

Supplements are everywhere and the evidence does not support them. Nutrition, physical activity, behavioral support, and where appropriate FDA-approved medication remain both more effective and considerably safer than whatever is currently being advertised.

Scott Rennie, D.O.

References

Thomas PR. Weight Loss Supplements. Columbia University Institute of Human Nutrition, 2022.

Geller AI et al. Emergency Department Visits for Adverse Events Related to Dietary Supplements. NEJM. 2015;373:1531-1540.

Tucker J et al. Unapproved Pharmaceutical Ingredients Included in Dietary Supplements Associated With US Food and Drug Administration Warnings. JAMA Network Open. 2018;1(6):e183337.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Do Weight Loss Apps and Devices Really Help?

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Patients ask me whether weight loss apps and digital programs actually work. It is a fair question, and the honest answer has a lot of qualifiers in it. Traditional obesity care runs into limited visit time, cost, and a shortage of places to refer people. Technology, whether an app, a web platform, or a hybrid program with human coaching, routes around some of that.

Dr. Bonnie Spring at Northwestern has studied how eHealth, mHealth, and telehealth are reshaping obesity treatment. Her finding is that these tools extend reach, lower cost, and deliver feedback in real time. The difficulty is holding anyone’s attention long enough for that to matter.

The trends in the research are reasonably clear. Web-based programs on their own produce small losses, around 2 to 3 percent of body weight. Better than nothing, and well short of the 7 to 8 percent that structured in-person programs achieve (Wieland 2014; Raaijmakers 2015; Tang 2014). Roughly half of users drop out.

Mobile approaches do better. In a review of U.S. trials, about 63 percent of studies found meaningful weight loss with mHealth interventions (Burke, Ma, Spring 2015). Texting on its own moved very little; outcomes improved when coaching or app-based monitoring was layered on. The catch is that most people abandon apps almost immediately, with more than three quarters stopping within three days of downloading.

Spring’s Opt-In Study used the Multiphase Optimization Strategy to build something cost-effective: remote sessions, structured self-monitoring, goal setting, and a trained buddy for support. Participants targeted a 7 percent loss, the threshold known to reduce diabetes and cardiovascular risk. More than half got there, at under $500 per person. That is comparable to the Diabetes Prevention Program at a fraction of the cost.

The buddy component turned out to matter most. Having a friend or family member reinforcing the changes between formal sessions kept people going, which lines up with what we already knew: social support is among the strongest predictors of durable results.

Access remains uneven. Reliable internet and comfort with digital tools are not evenly distributed, even though weight loss apps are among the most downloaded health apps in the world (Nikolaou & Lean, 2017). Owning a smartphone is the easy part. Cultural fit, affordability, and whether someone finds the technology tolerable all matter as much.

In my practice I have seen patients do well with commercial programs like Omada or Noom, which pair app-based tracking with remote coaching. Others get further with something simpler, MyFitnessPal being the usual example. These run somewhere between $40 and $130 a month, which is its own barrier and worth asking about before recommending one.

Technology works when it carries evidence-based strategy inside it: goal setting, self-monitoring, timely feedback, social support. Without those it is a download that gets deleted on day three. Knowing which products have research behind them and which have marketing behind them is part of our job now, and steering a patient toward the right one is often what separates a few weeks of enthusiasm from an actual result.

Scott Rennie, D.O.

References

Spring B. Use of Technology in the Prevention and Treatment of Obesity. Northwestern University, 2024.

Wieland LS et al. Systematic Reviews. 2014.

Raaijmakers LGM et al. Obesity Reviews. 2015.

Tang J et al. Obesity Reviews. 2014.

Burke LE, Ma J, Spring BJ et al. Ann Behav Med. 2015.

Nikolaou CK, Lean MEJ. Int J Obes. 2017.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

How to Sleep Better: Practical Steps for Patients

On By Dr. Scott RennieIn Other Diseases and ConditionsLeave a comment

Sleep gets a fraction of the attention we give diet and exercise, and it should not. Research from Dr. Ari Shechter at Columbia University has shown that poor sleep feeds obesity, diabetes, hypertension, and heart disease. It costs people their daily functioning, and underneath that it is quietly setting long-term disease risk. It is not a secondary problem.

When I ask patients about sleep, I keep it practical. When did this start, and is it new or has it always been like this? What is the bedroom like, too warm or too bright or too loud? Do they snore, gasp, or stop breathing, which points toward apnea? Any crawling or tingling in the legs, which points toward restless legs? I ask about weekdays versus weekends, because an irregular schedule can look exactly like insomnia. And I ask about caffeine, alcohol, nicotine, and medications, which patients rarely volunteer.

Formal tools give the conversation structure. The Epworth Sleepiness Scale is quick for daytime sleepiness. The Pittsburgh Sleep Quality Index is broader. STOP-Bang and the Berlin questionnaire flag possible apnea. The Insomnia Severity Index tracks both severity and how much it is costing someone functionally.

For objective data, in-lab polysomnography remains the standard for apnea, limb movement disorders, narcolepsy, and REM sleep behavior disorder. Wrist actigraphy at home gives a more practical picture of sleep and wake patterns over time, which is often what I actually need.

Adults should target 7 to 9 hours, and children and teenagers need more. Hours alone do not settle it. Timing, efficiency, and how someone feels the next day all matter. Patients tell me constantly that they are in bed for eight hours and wake up unrested. That is the point where efficiency and awakenings become the more useful thing to look at.

The consequences of chronic short sleep are well documented. It shifts ghrelin and leptin in the direction of more hunger and weight gain (Spiegel et al., 2004). It degrades glucose control and raises diabetes risk (Tasali et al., 2022). Hypertension, coronary disease, and stroke all track with insufficient sleep, and long-standing sleep problems are associated with cognitive decline and dementia risk (Vorster et al., 2024).

Causes are usually layered. Behavior contributes: irregular schedules, screens late, heavy meals and alcohol close to bed. So do physiologic and psychological factors: apnea, restless legs, anxiety, chronic pain.

Practical work starts with sleep hygiene. A consistent schedule resets circadian rhythm. Bedrooms should be cool, dark, and quiet. Bright light late interferes with sleep onset. Evening caffeine and alcohol come down. A wind-down routine, reading or stretching or a warm shower, makes the transition easier.

Daytime habits matter more than patients expect. Morning light anchors circadian rhythm. Even ten minutes of aerobic activity improves sleep depth. And for anyone waking in the night, what they do next shapes the rest of it: awake more than twenty minutes, get up and do something quiet in dim light rather than lie there getting frustrated.

The behavioral approach I use most is stimulus control. The principle is simple, which is rebuilding the association between the bed and sleep. Go to bed only when sleepy. Use the bed for sleep. Leave it if sleep is not coming. I have watched patients with years of insomnia retrain themselves this way. One had been scrolling his phone in bed for hours every night; once he started leaving the room when sleep would not come and only returning when he felt drowsy, his sleep onset shortened within a few weeks and the nightly frustration went with it.

Sleep is a medical necessity, and it belongs in routine care alongside everything else we screen for. Taking it seriously improves rest, and it also improves cardiometabolic health, mental health, and how people feel about their days.

Scott Rennie, D.O.

References

Shechter A. Improving Sleep in Your Patients. Columbia Cornell Obesity Medicine Course, 2024.

Spiegel K et al. Ann Intern Med. 2004.

Tasali E et al. JAMA Intern Med. 2022.

Markwald RR et al. PNAS. 2013.

Vorster A et al. Clin Transl Neurosci. 2024.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Does Chronic Stress Cause Weight Gain? A Doctor Explains

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Obesity gets described as a balance of diet and exercise, and stress plays a far larger role in it than most people are told. I have seen patients who eat well and stay active and still lose ground the moment their stress rises. Research from Dr. Rajita Sinha at Yale explains a good deal of why. Chronic stress produces measurable biological change, well past anything you would call a mood.

Stress acts on the brain circuits governing emotion, motivation, and self-control. Those circuits overlap with the ones handling food reward and craving, particularly for calorie-dense processed food (Sinha et al., 2022). Cortisol climbs under chronic stress. Ghrelin rises with it while leptin falls. What you end up with is a body primed to eat more, in an environment where high-calorie food is always within reach.

Calling that emotional eating undersells it. In Sinha’s lab work, people exposed to stress through guided imagery ate more snack food afterward, and participants who were already overweight were the most affected. Their cravings and calorie intake tracked with measured increases in cortisol and ghrelin. The stress reached past how they felt and changed how their brains and bodies handled food.

The pandemic ran this experiment at national scale. Nearly half of U.S. adults gained weight over that period, with worse effects among people who already had higher BMIs (Khubchandani et al., 2022). Children were not spared; CDC data showed the rate of BMI increase doubling against pre-pandemic years (Lange et al., 2021). The predictors of gain were emotional distress, having children at home, and how long it had been since someone last weighed themselves.

Work outside the pandemic points the same way. In one community study, people with higher baseline cortisol and greater insulin resistance were more likely to gain weight over the following six months (Chao et al., 2017). Those markers did more than correlate with obesity. They predicted it.

That has pushed researchers past the eat-less-move-more framing toward treatments aimed at the stress itself. Mindfulness-based stress reduction lowers food cravings, perceived stress, and blood pressure in people with obesity (Tuit et al., 2011). There is even evidence in parenting: a small study of low-income mothers found mindful parenting reduced parental stress and was associated with healthier BMI outcomes in their children (Jastreboff et al., 2018).

Medical and surgical treatment still matter, and the evidence suggests they perform best alongside strategies that reduce stress reactivity and support executive function. Stress management belongs in the treatment plan rather than tacked onto the end of it.

I have seen patients who feel defeated because they are certain the weight they gained under stress was a personal failure. The science says otherwise. Stress reshapes brain pathways, moves hormone levels, and changes eating behavior in ways we can measure. None of that makes change impossible. It does mean compassion is not optional in this conversation, and that treating stress as part of the disease moves the discussion off blame and onto something we can actually act on.

Scott Rennie, D.O.

References

Sinha R. Chronic Stress and Obesity. Yale School of Medicine, Columbia Obesity ABOM Virtual Course, 2022.

Chao A et al. High Cortisol and Insulin Resistance Predict Weight Gain. Obesity. 2017.

Khubchandani J et al. Depression and Anxiety Predict Weight Gain During the COVID-19 Pandemic. Diabetes & Metabolic Syndrome. 2022.

Lange SJ et al. Body Mass Index Increase in Children During COVID-19. MMWR Morb Mortal Wkly Rep. 2021.

Tuit K et al. Mindfulness and Stress Reduction in Obesity. Appetite. 2011.

Jastreboff AM et al. Mindful Parenting and Childhood Obesity Prevention. Journal of Pediatrics. 2018.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

How Weight Stigma Hurts Health and Makes Obesity Worse

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Conversations about obesity circle back to calories, exercise, and willpower almost every time. Weight stigma gets far less airtime and carries comparable weight. I have seen patients delay care or stop coming back entirely because of how they were treated somewhere else. The discomfort is the smaller part of it. The evidence says stigma itself worsens health and can contribute to weight gain.

Weight stigma is being stereotyped or discriminated against because of body size. It shows up in schools, workplaces, public spaces, and clinical settings. Dr. A. Janet Tomiyama’s work frames it as a chronic stressor, and stress is never metabolically neutral. It sets off hormonal changes that drive appetite and shift metabolism.

Her team built the COBWEBS model to describe the loop. Stigma triggers stress, cortisol rises, cravings intensify, calorie-dense food becomes more appealing, weight gain follows, and the weight gain brings more stigma (Tomiyama, 2014).

The measurements back the model. Women with higher BMIs who reported more stigma experiences had significantly higher morning cortisol than women at similar BMIs reporting fewer such experiences (Tomiyama et al., 2014). What separated the two groups was not their weight. It was how they had been treated.

Simulated experience shows it too. Participants who wore a fat suit to approximate living in a larger body reported more distress afterward and ate more calorie-dense snacks than controls (Heldreth et al., 2018). The premise that shaming people improves their health does not survive contact with the data. It usually produces the opposite.

The longitudinal picture is worse. Adolescent girls teased about their weight by family or peers had higher BMIs years later, holding self-esteem and body image constant (Hunger & Tomiyama, 2014). Stigma sits upstream of obesity as well as downstream. It forecasts it.

Healthcare has no exemption here. Clinicians who specialize in obesity medicine have been shown to carry implicit anti-fat bias, and patients pick up on it immediately. I have had patients tell me directly that they put off care because they did not want to be weighed or judged again. The literature matches what they describe: stigma in healthcare settings is associated with shorter visits, fewer diagnostic tests, and worse outcomes (Tomiyama et al., 2022).

It reaches providers as well. Medical students who internalize anti-fat bias have higher rates of depression and substance use. The damage runs in more than one direction.

Weight stigma is a health risk in its own right. It raises stress, fuels craving, keeps people away from care, and pushes outcomes the wrong way. What patients need is care aimed at behavior and health rather than at their size, and the work for us is examining our own language, our assumptions, and the spaces we ask people to walk into.

Scott Rennie, D.O.

References

Tomiyama AJ. Weight stigma is stressful: A review of evidence for the Cyclic Obesity/Weight-Based Stigma model. Appetite. 2014.

Tomiyama AJ et al. Health Psychology. 2014.

Heldreth CM, Incollingo Rodriguez AC, Tomiyama AJ. Obesity. 2018.

Hunger JM, Tomiyama AJ. JAMA Pediatrics. 2014.

Tomiyama AJ et al. Stigma and health outcomes in clinical settings. 2022.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Can Diet and Exercise Lower Cancer Risk in Obesity?

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

When obesity comes up, the conversation goes to diabetes, heart disease, and joints. Cancer rarely makes the list, and it belongs near the top of it. Obesity is an established risk factor for developing several cancers and for dying from them. Over the past twenty years the evidence has firmed up considerably that lifestyle change, cutting calories and adding endurance exercise in particular, lowers that risk and improves outcomes for patients already diagnosed.

The biology is messy and worth understanding anyway. Surplus calories expand fat tissue, and enlarged fat cells are metabolically active rather than inert. They drive systemic inflammation, disrupt insulin signaling, and shift leptin, insulin, and estrogen levels. The resulting environment is one cancer establishes itself in more easily. Longo and Fontana described how obesity suppresses protective factors like adiponectin and sex hormone-binding globulin while raising free fatty acids, inflammatory cytokines, and oxidative stress (Longo & Fontana, Trends Pharmacol Sci, 2010). That combination degrades DNA repair, lets mutated cells survive, and weakens immune surveillance.

The clinical consequences follow. Patients with obesity are more likely to develop breast and endometrial cancer, both hormone-sensitive. Insulin and IGF-1 push cells to keep dividing. Suppressed SHBG leaves more free estrogen circulating. Chronic inflammation supplies the rest. Tumors appear in that setting and then do well in it.

Caloric restriction has decades of animal work behind it. Rodents held at roughly 30 percent fewer calories lived longer with fewer tumors (Weindruch & Sohal, NEJM, 1997; Masoro, Mech Ageing Dev, 2005). Non-human primates showed the same pattern, and in one study moderate restriction halved cardiovascular and cancer deaths (Colman et al., Science, 2009). Human trials are shorter but pointed in the same direction: a two-year study cutting intake 13 percent improved insulin sensitivity, lowered fasting insulin, and reduced oxidative stress (Kraus et al., Lancet Diabetes Endocrinol, 2019).

Exercise moves the same levers by a different route. Endurance training improves glucose uptake in muscle through increased GLUT4 expression, trims visceral fat, and lowers fasting insulin. A year-long trial in middle-aged adults found regular endurance exercise reduced weight, visceral fat, and insulin (Weiss et al., Am J Clin Nutr, 2006). A single session improves insulin sensitivity temporarily, and the benefit is gone in about ten days without activity (McCoy et al., J Appl Physiol, 1994). That is the detail I bring up with patients who train hard for a month and then stop. Exercise also supports mitochondrial function and immune defense, both relevant to prevention.

Combined, the two do more than either alone. Look AHEAD followed adults with type 2 diabetes for over a decade and found 16 percent fewer obesity-related cancers among those who lost weight through lifestyle change (Look AHEAD Research Group, Obesity, 2020). Bariatric surgery, which is caloric restriction enforced surgically, halved cancer deaths in patients with obesity, most notably in women with insulin resistance (Adams et al., NEJM, 2007; Anveden et al., Gynecol Oncol, 2017).

Newer work is looking at protein and amino acid restriction. Limiting branched-chain amino acids slows tumor growth in animals, probably through mTOR signaling and immune effects (Fontana et al., Oncotarget, 2013; Orillion et al., Clin Cancer Res, 2018). Early days, but it may become another tool.

For patients the practical version is short. Modest calorie reduction and structured endurance exercise reverse a good many of the pathways connecting obesity to cancer. Around 13 percent calorie reduction looks safe and effective in human trials. For exercise, 150 to 300 minutes a week scaled to what someone can actually manage is a reasonable target. For clinicians, these belong in the core toolkit for prevention and survivorship rather than in the section of the plan we get to if there is time.

Scott Rennie, D.O.

References

Longo VD, Fontana L. Trends Pharmacol Sci. 2010.

Weindruch R, Sohal RS. Caloric intake and aging. NEJM. 1997;337(14):986-994.

Masoro EJ. Mech Ageing Dev. 2005.

Colman RJ et al. Science. 2009.

Kraus WE et al. Lancet Diabetes Endocrinol. 2019.

Weiss EP et al. Am J Clin Nutr. 2006.

McCoy M et al. J Appl Physiol. 1994.

Adams TD et al. NEJM. 2007.

Anveden Å et al. Gynecol Oncol. 2017.

Look AHEAD Research Group. Obesity. 2020.

Fontana L et al. Oncotarget. 2013.

Orillion A et al. Clin Cancer Res. 2018.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

How Obesity and Nutrition Affect Cancer Risk

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Nutrition tends to get treated as background noise in oncology, good for general health but peripheral to the actual treatment. That view is losing ground. Food behaves as information as much as fuel, shaping metabolism, influencing tumor biology, and affecting both cancer risk and outcomes.

Obesity is the clearest illustration. It is a metabolic state rather than a matter of extra weight. Higher BMI is linked to increased incidence and mortality across several cancers, breast, colon, and endometrial among them (Calle et al., NEJM, 2003). Excess adipose tissue alters hormones, raises inflammation, and activates growth pathways that hand tumors an advantage. Elevated insulin and IGF-1 drive proliferation. Leptin rises, adiponectin falls, and the balance tips toward growth. Adipose tissue also produces estrogen, which raises risk for the hormone-sensitive cancers (Schvartzman, 2023).

Cancer cell metabolism adds a layer. Rather than relying mainly on oxidative phosphorylation, many cancer cells run aerobic glycolysis, the Warburg effect, generating both energy and the building blocks for rapid division (PMID: 26232225). Which raises the obvious question of whether diet can be used to push back.

The evidence is mixed and growing. Ketogenic diets have shown potential for boosting immune responses against tumors (PMID: 27178315), while in renal cell carcinoma and BRAF-mutated melanoma they may promote growth instead (PMID: 28089569). Restricting amino acids such as methionine, or serine and glycine, slows tumor growth in preclinical work (PMID: 28425994, 32413275). High-dose vitamin C has shown promise in KRAS-mutant cancers (PMID: 26541605). And the gut microbiota, which diet shapes, appears to affect how well patients respond to immune checkpoint inhibitors (PMID: 29097494).

All of which points toward precision nutrition. What helps one cancer may do nothing for another, or worse. Tumor type, genetics, insulin sensitivity, concurrent treatment, and the microbiome all bear on it. So does whether a patient can actually live with the diet, because one that works in theory and not in practice has not helped anyone.

So what do I tell patients? Not to follow a cancer diet, because there is no such thing. I point them toward the findings that hold up consistently. Mediterranean-style eating and lower-carbohydrate patterns reduce inflammation and may lower recurrence risk (PMID: 28935150). Fiber supports the microbiome and helps hold metabolic balance (PMID: 29098294). Observational work links nuts, fish, olive oil, and coffee to lower cancer risk or mortality (PMID: 27436272, 29158191).

One patient I worked with had breast cancer and wanted to eat better without overhauling her life. We stayed with Mediterranean-style adjustments: more vegetables, legumes, fish, and olive oil, less in the way of processed food and added sugar. Her oncologist was on board. Through treatment she held her weight steady, had fewer energy crashes, and tolerated therapy better than she expected. None of that cured anything. It was a concrete thing she could do that supported the care she was getting, and it mattered to her that it was hers to do.

Obesity and nutrition influence cancer biology directly, through metabolic and inflammatory pathways we can measure. Nutrition is not a replacement for standard therapy and it should not be the last thing we get to either.

Scott Rennie, D.O.

References

Calle EE et al. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. NEJM. 2003;348(17):1625-1638. PMID: 12711737

Schvartzman JM. Metabolism, Nutrition, Obesity & Cancer. Columbia University Lecture, 2023.

Sullivan LB et al. Supporting aspartate biosynthesis is an essential function of respiration in proliferating cells. Cell. 2015. PMID: 26232225

Lussier DM et al. Enhanced immunity in a mouse model of malignant glioma is mediated by a therapeutic ketogenic diet. BMC Cancer. 2016. PMID: 27178315

Xia S et al. Prevention of dietary-fat-fueled ketogenesis attenuates BRAF V600E tumor growth. Cell Metab. 2017. PMID: 28089569

Maddocks ODK et al. Modulating the therapeutic response of tumours to dietary serine and glycine starvation. Nature. 2017. PMID: 28425994

Lien EC, Vander Heiden MG. Dietary approaches to cancer therapy. Cancer Cell. 2020. PMID: 32413275

Yun J et al. Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH. Science. 2015. PMID: 26541605

Routy B et al. Gut microbiome influences efficacy of PD-1-based immunotherapy against epithelial tumors. Science. 2018. PMID: 29097494

Farinetti A et al. Mediterranean diet and colorectal cancer: A systematic review. Nutrition. 2017. PMID: 28935150

Song M et al. Fiber intake and survival after colorectal cancer diagnosis. JAMA Oncol. 2018. PMID: 29098294

Song M et al. Marine ω-3 polyunsaturated fatty acid intake and survival after colorectal cancer diagnosis. Gut. 2017. PMID: 27436272

Hu Y et al. Association between coffee intake after diagnosis of colorectal cancer and reduced mortality. Gastroenterology. 2018. PMID: 29158191

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.