The August Evidence Edit
What I’m Reading, and How It’s Changing My Clinical Practice
As August comes to an end, I’ve spent a good portion of my summer doing something that has always been incredibly important to me professionally: continuing to learn.
I’ve been taking courses, reviewing clinical practice guidelines, reading systematic reviews and meta-analyses, and digging into newer research in women’s health, metabolic health, cardiovascular disease, body composition and nutrition.
There is more nutrition information available than ever before, but more information does not necessarily mean better information.
My role as a Registered Dietitian is not simply to follow the newest headline. It is to ask:
How strong is the evidence?
Who was actually studied?
How meaningful was the effect?
And most importantly, how should this change what we actually do?
Here are some of the findings that have stood out to me most.
1. MENOPAUSE
The focus needs to shift from simply losing weight to protecting muscle, bone and metabolic health.
Menopause is increasingly being understood as a window of opportunity for prevention; not simply a stage during which women need to “eat less.”
A 2023 systematic review and meta-analysis examining 101 studies involving 5,697 postmenopausal women found that exercise training improved muscle mass and fat-free mass while reducing fat mass, body-fat percentage, waist circumference and visceral fat.
Resistance and combined aerobic/resistance training were particularly beneficial for preserving and building muscle.
A separate 2024 systematic review and meta-analysis found that resistance training significantly improved both upper- and lower-body strength in postmenopausal women.
WHAT THE EVIDENCE IS TELLING US
The menopause conversation should not simply be: “How do I weigh less?”
It should increasingly become:
“How do I improve body composition while protecting muscle, bone, strength and long-term metabolic health?”
Also, WHAT SWAN HAS TAUGHT US ABOUT MENOPAUSE
The landmark Study of Women’s Health Across the Nation (SWAN) has followed thousands of women through midlife and has fundamentally changed how we understand menopause.
Some of its most striking findings:
• ~80% of women reported hot flashes or night sweats at some point during the menopause transition.
• 7.4 years was the median duration of frequent hot flashes/night sweats—not simply a few months.
• ~2 years before the final menstrual period, the rate of fat gain doubled while lean mass began to decline—even though the scale did not show the same dramatic shift.
• Bone loss accelerates around menopause, with the most rapid decline occurring approximately 1 year before through 2 years after the final menstrual period.
How this translates into my clinical practice
1. Protein becomes more intentional.
Rather than allowing most protein to accumulate at dinner, I want meaningful protein opportunities throughout the day.
2. Breakfast matters.
A coffee and piece of toast provides a very different protein stimulus than a breakfast containing approximately 25–35 g of high-quality protein.
3. Resistance training becomes part of the nutrition conversation.
Nutrition and exercise should not operate in separate silos.
4. We measure more than weight.
Waist circumference, strength, body composition, bloodwork, energy and physical function can provide much more meaningful information.
5. Aggressive restriction is rarely the goal.
During midlife, protecting lean tissue becomes increasingly important.
Selected References
Sá, K. M. M., da Silva, G. R., Martins, U. K., et al. (2023). Resistance training for postmenopausal women: Systematic review and meta-analysis. Menopause, 30(1), 108–116. doi:10.1097/GME.0000000000002079.
González-Gálvez, N., Moreno-Torres, J. M., & Vaquero-Cristóbal, R. (2024). Resistance training effects on healthy postmenopausal women: A systematic review with meta-analysis. Climacteric, 27(3), 296–304. doi:10.1080/13697137.2024.2310521.
The effects of exercise training on body composition in postmenopausal women: A systematic review and meta-analysis. (2023). Frontiers in Endocrinology, 14, 1183765.
Greendale, G. A., Sternfeld, B., Huang, M., Han, W., Karvonen-Gutierrez, C., Ruppert, K., Cauley, J. A., Finkelstein, J. S., Jiang, S.-F., & Karlamangla, A. S. (2019). Changes in body composition and weight during the menopause transition. JCI Insight, 4(5), e124865.
2. FERRITIN + IRON
The “energy marker” I think deserves far more attention in women.
This is one of the laboratory markers I pay particularly close attention to in women.
Ferritin provides an estimate of the body’s iron stores; and iron deficiency can exist long before hemoglobin falls into the anemia range.
In other words:
You do not have to be anemic to be iron deficient.
A major Canadian clinical review published in CMAJ in 2025 highlighted just how common this is. An Ontario study cited in the review estimated that among screened nonpregnant females: 38% had non-anemic iron deficiency.13% had iron-deficiency anemia.
Another Canadian population analysis found iron deficiency in approximately 18% of women aged 19–50, with estimates varying depending on the definition used.
Menstrual blood loss is one of the biggest contributors.
The same Canadian review notes that approximately 18–50% of females may meet criteria for heavy menstrual bleeding, which remains substantially underdiagnosed.
WHY I SOMETIMES CALL FERRITIN AN “ENERGY MARKER”
Iron is involved in oxygen transport, mitochondrial energy production, neurological function and neurotransmitter pathways.
Iron deficiency, with or without anemia, has been associated with symptoms including:
fatigue
reduced exercise tolerance
difficulty concentrating
cognitive changes or “brain fog”
irritability
headaches
hair changes
restless legs
reduced quality of life
Importantly, these symptoms are nonspecific. Low energy does not automatically mean low ferritin, but ferritin is certainly worth investigating when the clinical picture fits.
WHAT NUMBER MATTERS?
This requires some nuance.
A ferritin below 30 µg/L is a well-established threshold for iron deficiency in most adults.
However, the newer Canadian review notes that ferritin below 50 µg/L has physiologic relevance, corresponding with other biochemical signs of iron depletion and increased intestinal iron absorption.
In fact, in 2024 several large Canadian laboratories raised their lower reference limit for ferritin to better identify clinically important deficiency.
What about a ferritin above 100?
A useful distinction from the 2025 Canadian review is:
Oral iron treatment target: ferritin ≥50 µg/L
Following IV iron: ferritin ≥100 µg/L may be used as a treatment target, particularly because these patients often have a greater risk of rapid iron-store depletion.
THE FINDING I WANT MORE WOMEN TO KNOW
“Normal hemoglobin” does not rule out iron deficiency.
A CBC and ferritin should be interpreted together, and when inflammation is suspected, transferrin saturation and other iron indices may also be useful.
How do we actually increase ferritin?
STEP 1: Find out why it is low.
Simply prescribing iron over and over without investigating the cause misses half the clinical picture.
Potential contributors include:
heavy menstrual bleeding
pregnancy/postpartum iron depletion
low dietary iron intake
frequent blood donation
gastrointestinal blood loss
celiac disease
inflammatory bowel disease
bariatric surgery
impaired absorption
medications or conditions affecting gastric acidity
STEP 2: Increase dietary iron.
Higher-bioavailability heme iron:
beef
poultry
seafood
shellfish
Plant-based iron:
lentils
beans
tofu
edamame
pumpkin seeds
iron-fortified foods
Pairing plant iron with vitamin-C-rich foods can enhance absorption.
Coffee, tea and large calcium doses taken at the same eating occasion can reduce non-heme iron absorption.
STEP 3: Oral iron when indicated
Oral iron remains first-line treatment for many people.
A comprehensive 2024 review concluded that traditional ferrous salts remain inexpensive and effective first-line options, although gastrointestinal side effects frequently limit adherence.
Common formulations include:
Ferrous sulfate = Very well studied and inexpensive.
Ferrous fumarate = Also effective and commonly used in Canada.
Ferrous gluconate = Provides less elemental iron per tablet but may be useful depending on dosing and tolerance.
Polysaccharide iron complex = Sometimes chosen for tolerability, although being more expensive does not automatically mean it will raise ferritin more effectively.
Ferric maltol = A newer oral option with evidence for improving hemoglobin and iron indices, particularly in populations such as inflammatory bowel disease and chronic kidney disease.
What matters most is:
appropriate elemental iron dose
absorption
tolerability
consistency
correction of the underlying cause
An important shift: more iron isn't always better.
Higher doses can produce more gastrointestinal symptoms and can increase hepcidin, which temporarily reduces iron absorption.
For some patients, lower-dose or alternate-day oral iron may improve absorption and tolerability compared with repeatedly taking large doses throughout the day.
STEP 4: Know when oral iron isn't working.
This is something I increasingly encourage women to discuss with their medical team.
IV iron may be appropriate when there is:
intolerance to oral iron
inadequate response despite adherence
malabsorption
inflammatory gastrointestinal disease
continued substantial blood loss
need for faster iron replacement
certain pregnancy/postpartum situations
iron-deficiency anemia that cannot realistically be corrected orally
The 2025 Canadian review specifically states that IV iron is useful when oral iron cannot be tolerated, in malabsorption states and when rapid replacement is clinically necessary.
In Canada, examples include:
Monoferric® ferric derisomaltose
Ferinject® ferric carboxymaltose
Venofer® iron sucrose
Monoferric is Health Canada–approved for adults with iron-deficiency anemia who have intolerance or an inadequate response to oral iron therapy.
These are prescription therapies with specific indications, contraindications and monitoring requirements; not simply a faster supplement.
My clinical takeaway
If someone's ferritin repeatedly remains very low despite appropriate oral therapy; or they cannot tolerate oral iron; I want that conversation to continue rather than simply accepting chronic iron deficiency as “normal for women.”
Selected References
Sholzberg, M., Hillis, C., Crowther, M., & Selby, R. (2025). Diagnosis and management of iron deficiency in females. CMAJ, 197(24), E680–E687. doi:10.1503/cmaj.240570.
Cooper, M., Greene-Finestone, L., Lowell, H., & Levesque, J. (2023). Population iron status in Canada: Results from the Canadian Health Measures Survey 2012–2019. Journal of Nutrition.
Pantopoulos, K. (2024). Oral iron supplementation: New formulations, old questions. Haematologica, 109(9), 2790–2801. doi:10.3324/haematol.2024.284967.
Miller, J. L., et al. (2024). Iron deficiency anemia among women: An issue of health equity. Blood Reviews, 64, 101159. doi:10.1016/j.blre.2023.101159.
3. INSULIN RESISTANCE
Insulin resistance is important, but the internet has oversimplified it.
Insulin resistance describes a state in which tissues such as skeletal muscle, liver and adipose tissue become less responsive to insulin.
The pancreas compensates by producing more insulin in an attempt to maintain normal glucose levels.
That means someone can potentially have:
normal glucose + increased insulin demand before glucose abnormalities become obvious.
But how is insulin resistance diagnosed?
This is where clinical nuance matters.
There is no universally accepted HOMA-IR cutoff that diagnoses insulin resistance in every population. The hyperinsulinemic-euglycemic clamp remains the research gold standard but is not practical for routine clinical care.
Fasting insulin and HOMA-IR may provide additional clinical information in selected circumstances, but interpretation depends on the laboratory, population and clinical context.
A 2025 systematic review involving 87 studies and more than 235,000 participants estimated a global insulin-resistance prevalence of approximately 26.5%, while also demonstrating enormous heterogeneity between studies—partly because diagnostic definitions vary.
WHAT THE EVIDENCE IS TELLING US
Insulin resistance is clinically important.
But: “My insulin is high, therefore my body cannot lose fat” is not an evidence-based conclusion.
Weight regulation remains influenced by appetite biology, caloric intake, energy expenditure, genetics, medications, sleep, food environment, muscle mass and many other factors.
What I assess clinically
Rather than interpreting one value alone, I often consider:
fasting glucose
HbA1c
fasting insulin when clinically useful
triglycerides
HDL-C
waist circumference
blood pressure
liver enzymes
family history
medication history
symptoms and overall metabolic phenotype
Nutrition strategies with evidence behind them
1. Increase dietary fibre.
A 2025 meta-analysis of 51 randomized trials involving 3,420 participants found fibre interventions reduced fasting glucose, fasting insulin and HOMA-IR in adults with overweight or obesity without diabetes.
2. Improve carbohydrate quality.
A 2025 meta-analysis found lower-glycemic dietary patterns improved HOMA-IR compared with higher-glycemic diets in adults without diabetes.
3. Pair carbohydrates with protein, fibre and healthy fats.
4. Build or preserve muscle.
Muscle is an important site for glucose disposal.
5. Move after meals.
Even relatively brief activity after eating can help reduce post-meal glucose exposure.
Selected References
Ballena-Caicedo, J., et al. (2025). Global prevalence of insulin resistance in the adult population: A systematic review and meta-analysis. Frontiers in Endocrinology, 16, 1646258. doi:10.3389/fendo.2025.1646258.
Wang, H., Cheng, R., Xie, L., & Hu, F. (2024). Comparative efficacy of exercise training modes on systemic metabolic health in adults with overweight and obesity: A network meta-analysis of randomized controlled trials. Frontiers in Endocrinology, 14, 1294362. doi:10.3389/fendo.2023.1294362.
4. CHOLESTEROL + Lp(a)
Your standard cholesterol panel may not tell the whole story.
One of the biggest shifts in cardiovascular prevention is growing attention to lipoprotein(a), or Lp(a).
Lp(a) is largely genetically determined.
Unlike LDL cholesterol, lifestyle usually has relatively little influence on the Lp(a) concentration itself.
That does not make lifestyle irrelevant.
It means that if Lp(a) is elevated, we become even more aggressive about controlling the cardiovascular risk factors we can modify.
THE CLINICAL-PRACTICE CHANGE
Canadian Cardiovascular Society guidance recommends:
“measuring Lp(a) level once in a person’s lifetime”
as part of initial lipid screening.
Elevated Lp(a); particularly ≥50 mg/dL or ≥100 nmol/L can meaningfully affect cardiovascular risk assessment.
What I increasingly like to see
Not simply:
total cholesterol
LDL-C
HDL-C
triglycerides
but when appropriate:
non-HDL cholesterol
ApoB
Lp(a)
HOW MUCH CAN LDL ACTUALLY CHANGE?
This is where nutrition becomes fascinating because several modest changes can become powerful when combined.
Evidence-based LDL-lowering strategies include:
Replacing saturated fats with unsaturated fats
Increasing soluble/viscous fibreThink oats, barley, beans, lentils and psyllium.
Plant sterols
Nuts and seeds
Replacing some animal protein with plant proteins
Soy protein
A 2024 meta-analysis of 63 randomized controlled trials found soy protein supplementation produced modest but significant reductions in LDL-C and total cholesterol.
The Portfolio dietary pattern intentionally combines several cholesterol-lowering foods; viscous fibre, plant protein, nuts and plant sterols; creating a cumulative effect much greater than any single “superfood.”
The takeaway
LDL reduction is rarely about removing one food.
It is about stacking several evidence-based interventions.
And when genetically driven risk such as elevated Lp(a) exists, lifestyle and medication management should work together rather than compete with each other.
Selected References
Pearson, G. J., Thanassoulis, G., Anderson, T. J., et al. (2021). 2021 Canadian Cardiovascular Society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in adults. Canadian Journal of Cardiology, 37(8), 1129–1150.
Effects of high-quality protein supplementation on cardiovascular risk factors in individuals with metabolic diseases: A systematic review and meta-analysis of randomized controlled trials. (2024). Clinical Nutrition.
5. FATTY LIVER; NOW MASLD
A fatty liver is often giving us information about metabolic health before symptoms appear.
What was previously commonly called NAFLD is now referred to as:
Metabolic dysfunction-associated steatotic liver disease, MASLD.
The 2024 European multidisciplinary clinical practice guideline emphasizes dietary quality, exercise, weight management where appropriate, cardiometabolic risk management and, critically, identifying people at risk for liver fibrosis.
A PRACTICE-CHANGING POINT
Normal or mildly elevated liver enzymes do not reliably tell us whether significant fibrosis is present. The guideline recommends beginning risk assessment with a non-invasive calculation such as:
FIB-4
followed by elastography or another validated assessment when indicated.
Nutrition matters, even without a “liver detox.”
The guideline specifically recommends:
Mediterranean-style dietary patterns
minimizing sugar-sweetened beverages
reducing ultra-processed foods
reducing excess saturated fat
emphasizing minimally processed foods
regular physical activity
What about carbohydrates?
It is overly simplistic to say:
“Carbs cause fatty liver.”
I care much more about:
total energy intake
refined carbohydrate load
added sugars
sugar-sweetened beverages
fibre
carbohydrate quality
portion size
overall dietary pattern
For some clients, structuring starch portions across eating occasions rather than having very large carbohydrate loads at one meal can also make the plan easier to manage metabolically.
AND YES, COFFEE IS INTERESTING.
Observational evidence consistently associates coffee consumption with more favourable liver outcomes and lower fibrosis risk.
The 2024 MASLD guideline specifically acknowledges this relationship.
But this needs to be interpreted correctly:
Coffee is associated with better liver outcomes. It is not a prescribed treatment for MASLD.
Selected References
European Association for the Study of the Liver, European Association for the Study of Diabetes, & European Association for the Study of Obesity. (2024). EASL–EASD–EASO clinical practice guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). Journal of Hepatology.
6. INTERMITTENT FASTING
The eating window isn't magic. What happens inside it matters.
Intermittent fasting and time-restricted eating can be useful tools for some people.
But the research is much more nuanced than:
“Fasting burns more fat.”
A 2025 meta-analysis of 20 randomized controlled trials involving 1,242 participants found that time-restricted eating reduced body weight and fat mass, but also produced a reduction in fat-free mass.
Adding time-restricted eating to an already calorie-restricted diet did not appear to create a large additional weight-loss advantage.
WHAT THE EVIDENCE IS TELLING US
The question is not:
“Should everyone fast?”
It is:
“Does this eating schedule help this particular person meet their nutritional requirements while protecting muscle and supporting metabolic health?”
If an eight-hour window results in:
skipping protein-rich meals
chronically under-eating
consuming nearly all protein at dinner
poor workout recovery
inadequate vitamins and minerals
then I am much less interested in the fact that the person technically “fasted.”
If someone prefers time-restricted eating
I focus on:
1. Adequate overall energy intake
2. Adequate total protein
3. Several meaningful protein opportunities
4. Resistance training
5. Monitoring lean mass and strength, not simply scale weight
Selected References
He, M., Li, B., Li, M., & Gao, S. (2024). Does early time-restricted eating reduce body weight and preserve fat-free mass in adults? A systematic review and meta-analysis of randomized controlled trials. Diabetes & Metabolic Syndrome, 18(2), 102952. doi:10.1016/j.dsx.2024.102952.
Efficiency of time-restricted eating and energy restriction on anthropometrics and body composition in adults: A systematic review and meta-analysis of randomized controlled trials. (2025).
7. PROTEIN THRESHOLDS
Protein thresholds matter, but they are not a hard ceiling.
Research supports consuming a meaningful dose of high-quality protein at each meal to maximize muscle protein synthesis.
A practical target for many adults is:
Meals: ~25–40 g protein
Snacks: ~10–20 g protein
For older adults, people in menopause, and those trying to preserve muscle during weight loss, approximately 0.3–0.4 g protein/kg per meal is a useful evidence-based target.
WHAT THE EVIDENCE IS TELLING US
The goal is to reach a minimum effective protein dose at each eating occasion.
But protein above 30–40 g is not “wasted.” It is still digested, absorbed and used throughout the body.
Clinically, the bigger issue is usually protein distribution: many people eat very little protein at breakfast and lunch, then most of their protein at dinner.
My focus is therefore:
adequate total protein
enough protein per meal
even distribution across the day
resistance training
Selected References
Hettiarachchi, J., Reijnierse, E. M., Kew, N., Fetterplace, K., Tan, S.-Y., & Maier, A. B. (2024). The effect of dose, frequency, and timing of protein supplementation on muscle mass in older adults: A systematic review and meta-analysis. Ageing Research Reviews, 99, 102325. doi:10.1016/j.arr.2024.102325.
8. SOY
One of the most persistent hormone myths is not holding up to the evidence.
People frequently ask:
“Should women avoid soy because of estrogen?”
Soy contains isoflavones, which are classified as phytoestrogens.
But phytoestrogens are not equivalent to human estrogen.
This distinction matters.
A major 2025 systematic review and meta-analysis evaluated 40 randomized trials involving 3,285 postmenopausal women.
Researchers examined:
estradiol
FSH
endometrial thickness
vaginal maturation
Their conclusion was striking:
“Soy isoflavones had no statistically significant effect on any measure of estrogenicity.”
The certainty of evidence was rated moderate to high.
WHAT THE EVIDENCE IS TELLING US
Soy does not behave in the body like simply taking estrogen.
And that makes foods such as:
tofu
edamame
tempeh
fortified soy milk
soybeans
very useful sources of high-quality plant protein.
Soy also has cardiovascular benefits. A 2024 meta-analysis of randomized trials found soy protein supplementation modestly reduced LDL cholesterol and total cholesterol.
And for muscle? A 2025 meta-analysis of 43 randomized trials found no significant difference between soy protein and milk protein for muscle-mass outcomes.
Selected References
Viscardi, G., Back, S., Ahmed, A., et al. (2025). Effect of soy isoflavones on measures of estrogenicity: A systematic review and meta-analysis of randomized controlled trials. Advances in Nutrition, 16(1), 100327. doi:10.1016/j.advnut.2024.100327.
Gençtürk, N., Bilgiç, F. Ş., & Ulaşlı Kaban, H. (2024). The effect of soy isoflavones given to women in the climacteric period on menopausal symptoms and quality of life: Systematic review and meta-analysis of randomized controlled trials. Explore, 20(6), 103012. doi:10.1016/j.explore.2024.05.010.
Reid-McCann, R. J., Brennan, S. F., Ward, N. A., et al. (2025). Effect of plant versus animal protein on muscle mass, strength, physical performance, and sarcopenia: A systematic review and meta-analysis of randomized controlled trials. Nutrition Reviews, 83(7), e1581–e1603. doi:10.1093/nutrit/nuae200.
9. PROTEIN POWDERS
Whey versus plant: what actually matters?
Protein powder is not mandatory. I consider it a convenience tool. Someone who can consistently meet their protein requirements through food may not need it.
But for a person who:
struggles with breakfast
exercises early in the morning
has reduced appetite
is taking an appetite-reducing medication
requires relatively high protein
travels frequently
protein powder can be extremely useful.
Whey protein
Whey has:
excellent digestibility
high essential amino acid content
naturally high leucine content
making it particularly effective for stimulating muscle protein synthesis.
Soy protein
Soy is also a complete, high-quality protein.
The 2025 meta-analysis comparing plant and animal protein found no significant difference between soy and milk proteins for muscle-mass outcomes.
Other plant proteins
Pea, rice and blended plant products can absolutely contribute effectively.
For some isolated non-soy plant proteins, a slightly larger protein dose or combination of complementary proteins may help provide adequate essential amino acids and leucine.
What I actually look for on a protein powder
~20–30 g protein per serving
Good amino-acid quality
Relatively low added sugar
An ingredient list the person tolerates
Third-party testing, particularly for competitive athletes
And perhaps most importantly:
A flavour and texture they will actually use.
Because the scientifically “perfect” protein powder sitting untouched in the cupboard isn't particularly effective.
Selected Reference
Reid-McCann, R. J., Brennan, S. F., Ward, N. A., et al. (2025). Effect of plant versus animal protein on muscle mass, strength, physical performance, and sarcopenia: A systematic review and meta-analysis of randomized controlled trials. Nutrition Reviews, 83(7), e1581–e1603. doi:10.1093/nutrit/nuae200.
10. BONE HEALTH
Calcium and vitamin D are important, but modern osteoporosis care goes much further.
Bone health becomes particularly important through the menopause transition and beyond.
And one of the most interesting advances is that osteoporosis medications now fall into two very different categories.
Antiresorptive therapies
These slow the breakdown of bone.
Examples include:
bisphosphonates
denosumab
raloxifene
Anabolic therapies
These can actually stimulate new bone formation.
Examples include:
teriparatide
romosozumab
The 2023 Canadian Osteoporosis Guideline recommends considering specialist consultation regarding anabolic therapy for individuals at very high fracture risk; for example, those with a recent severe vertebral fracture or multiple vertebral fractures plus osteoporosis.
A STATISTIC WORTH KNOWING
In appropriate patients, approximately three years of bisphosphonate therapy results in an estimated:
20–30 fewer vertebral fractures
10 fewer nonvertebral fractures
and approximately
3 fewer hip fractures
per 1,000 people treated compared with no treatment.
Nutrition still matters enormously.
My bone-health framework includes:
Adequate calcium
Adequate vitamin D
Adequate protein
Resistance training
Weight-bearing activity
Avoiding chronic under-fuelling
But when osteoporosis or high fracture risk exists:
nutrition complements medical treatment, it does not replace it.
Selected References
Morin, S. N., Feldman, S., Funnell, L., et al. (2023). Clinical practice guideline for management of osteoporosis and fracture prevention in Canada: 2023 update. CMAJ, 195(39), E1333–E1348.
Osteoporosis Canada. (2023). Clinical practice guideline for management of osteoporosis and fracture prevention in Canada: 2023 update.
11. GLP-1 + GIP/GLP-1 MEDICATIONS
The goal should not simply be weight loss. It should be better-quality weight loss.
GLP-1 and dual GIP/GLP-1 medications, including semaglutide and tirzepatide, have fundamentally changed obesity and diabetes treatment.
But an increasingly important question is:
What tissue are we losing?
A major 2026 systematic review and meta-analysis examined 20 randomized controlled trials involving 15,782 participants.
Lean mass accounted for approximately:
35.2% of total weight lost with semaglutide
25.4% with tirzepatide
26.8% with liraglutide
Lifestyle interventions without resistance training showed a similar proportion of lean-mass loss: 26.2%.
But here is the finding I think is most clinically important:
Lifestyle intervention + resistance training:
only ~17.5% of total weight loss came from lean mass.
WHAT THE EVIDENCE IS TELLING US
The takeaway is not:
“GLP-1 medications destroy your muscle.”
Meaningful weight loss from almost any method usually includes some loss of lean tissue.
The better clinical question is:
How do we maximize fat loss while minimizing unnecessary losses of muscle, strength and function?
My nutrition priorities when someone is using these medications
1. Protein becomes even more important.
Reduced appetite can make accidental protein underconsumption extremely easy.
2. Protein first.
When appetite is limited, prioritize the most nutritionally valuable part of the meal.
3. Don't wait until dinner.
Aim for meaningful protein across the day.
4. Resistance training should accompany treatment whenever medically appropriate.
5. Avoid chronic severe under-fuelling.
Less appetite does not eliminate the body's need for protein, essential fats, vitamins and minerals.
6. Monitor more than weight.
Think:
strength
physical function
waist circumference
protein intake
body composition where useful
energy
nutrient adequacy
A 2025 meta-analysis examining dietary weight loss similarly found that adding resistance exercise helped protect fat-free mass while increasing fat-mass loss, reinforcing that this principle extends well beyond medication-assisted weight loss.
Selected References
Lean mass changes with incretin therapy versus lifestyle intervention: A systematic review and meta-analysis of randomised controlled trials. (2026). Diabetes, Obesity and Metabolism. doi:10.1111/dom.70666.
Effect of resistance exercise on body composition, muscle strength and cardiometabolic health during dietary weight loss in people living with overweight or obesity: A systematic review and meta-analysis. (2025).
WHAT ALL OF THIS RESEARCH HAS REINFORCED FOR ME
After spending so much of this summer reviewing the literature, I keep coming back to a surprisingly simple conclusion:
Evidence-based nutrition is becoming less about restriction, and much more about optimization.
Protect muscle.
Strength train.
Prioritize protein, but individualize the dose.
Pay attention to iron before anemia develops.
Eat more plants.
Increase fibre.
Use carbohydrates strategically rather than fearing them.
Know your cardiovascular numbers, including Lp(a) when appropriate.
Look beyond liver enzymes when metabolic liver disease is a concern.
Protect bone before the first fracture occurs.
And when medications can meaningfully improve health, use nutrition and exercise alongside them, not instead of them.
Most importantly:
There is no single perfect diet.
No single fasting window.
No universal carbohydrate target.
No magical protein number.
No supplement that replaces an individualized assessment.
The role of evidence-based nutrition care is to take everything we are learning from the research and ask:
What actually applies to the person sitting in front of me?
That is what continues to drive my clinical practice, and why continuing education will always remain such an important part of the work I do.
Here’s to continuing to learn, question, evolve and turn better science into better care!
Alissa Steinberg RD CDE MHSc
Registered Dietitian | Certified Diabetes Educator | Menopause Society Practitioner Candidate
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