A question often asked is “can you lose fat on a Ray Peat diet?”… “And if so, how does one go about doing so correctly?”.
The main reason for this article is to address the well-known fact that “excess” fatty oxidation is bad and that we want to rely mostly on glucose oxidation for fuel. So according to this concept, going into a caloric deficit is bad since it increases total fat oxidation.
And the “safe” way to lose fat is to allow the liver to excrete/detox fat, mainly polyunsaturated fat through glucuronidation.
So in this article I want to show you that we burn fat all the time and that we don’t have to be afraid to burn fat. It’s unavoidable.
As a disclaimer, there is no such thing as a Ray Peat diet. He discusses concepts of what’s bad and good and suggests the consumption of certain foods. It’s always up to the individual to find what works best for them.
Going into a deficit is not the same as overeating on fats. The body might upregulate fat oxidation because there are insufficient calories coming from the diet. High-fat diets, consisting mainly of PUFAs, promote inflammation, excess fat oxidation, insulin resistance, etc, whereas a deficit doesn’t necessarily.
A caloric deficit isn’t the same as a high fat diet, especially if your carb intake is high and the deficit small.
Let’s say 60% of your diet consists of carbs, 20% from protein and 20% from fat and you’re eating 2500 calories. That would be 55.5g of fat per day. If you reduce your calories by 300 and keep the macros the same, it would end up at 2200 calories per day and 48.8g of fat. But now your body has to make up for that 300 calorie loss and will mobilize 300 calories from adipose tissue stores. That will be 6.7g of fat. So basically, you’re back to 55.5g of fat. Total fat intake remains the same.
Is 55.5g a high fat diet? Not at all.
Will 55.5g of fat per day make you insulin resistant? Most likely not.
The problem with long-term, big calorie deficits are the reduction in metabolic rate and increase in stress hormones. But most of this occurs due to low carb intake. So keeping carbs as high as possible will help to prevent the negatives of a deficit.
Concept 2 – Can you burn glucose all the time?
To determine that we have to look at the respiratory quotient (RQ).
The RQ is the ratio of CO2 (carbon dioxide) production vs O2 (oxygen) consumption. An RQ of 1 indicates 100% carb oxidation, while a general value of 0.7 indicates 100% fatty acid oxidation (the value ranges between 0.69 and 0.73, depending on the oxidized fatty acid’s carbon chain length).
To produce the same amount of ATP, oxidation of fatty acids requires more oxygen than the oxidation of carbs. For example, the complete oxidation of one molecule of glucose requires 6 molecules of oxygen, while the complete oxidation of stearic acid requires 26 molecules of oxygen (R).
The RQ can actually go higher than 1 and that’s generally achieved by very high carb intake when CO2 production is increased over the amount of O2 intake. So this can be due to super-fast glucose oxidation. And for those that do not know, carbohydrates are the only macro that regulates its own oxidation. The more carbs you eat, the more you burn. You don’t have to earn it. And that’s because there is limited storage for glucose, so the body has to get rid of it.
And it’s not just the carb to fat ratio, but also protein to carb ratio. Eating too much protein at the expense of carbs also lowers RQ.
The question arises if we can maintain an RQ of 1.
The answer is no.
Different carb ratios and RQ
On a 30% carb diet, the average fasting RQ typically is approximately 0.80 and increases to 0.90 when carb intake is increased to 60% (R). This indicates a doubling of resting carb oxidation. I’d assume that fed RQ would be at 1 or higher, so depending on how frequently you eat, you might be able to maintain an RQ of 1 or at least close to 1.
So our first clue to optimizing the metabolism is to get close to or higher than 60% of our calories from carbs. I like 60%, since then protein and fat intake is still at a reasonable level for muscle gains and diet enjoyment.
This study found that, during a 30% deficit, carb intake of roughly 77% total calories created a 24h RQ of 0.85 (R). The high carb diet had a very low fat intake, but due to the large deficit, their RQ wasn’t that high.
|Low carb||High carb|
The high carb group’s RQ was 0.85 before going into a deficit and their carb intake was at 50%. After going into a deficit and bumping it up to 71%, their RQ remained the same. And if you look at the data, even though RQ remained the same, carb oxidation increased and fat oxidation decreased. And despite that fact, they still lost more fat and the low carb group (89±6 g/d vs 53±6 g/d of body fat loss).
The only thing is that this study was short-term, only 6 days, but regardless, it shows that carb intake needs to be at least around 350g to have a 24h RQ of 0.85. High carb or smaller deficit is needed to keep the RQ high.
Here are some more data from that study if you want to have a look. The RC is reduced carb and the RF is reduced fat.
So as you can see from the study, even by going into a 30% deficit didn’t increase total fat oxidation. The fat that they removed from the diet was mobilized from the adipose tissue, thus putting them close to a 0% change. In other words, a deficit doesn’t equal a high-fat diet. Just make sure your carb intake is high.
Protein to carb ratio and RQ
Protein also has an inhibitory effect on glucose oxidation, so it’s important not to keep it too high.
This study found that natural bodybuilders on a high protein (25% of total calories) ketogenic diet had an RQ of 0.79. And the group that was eating 55% of their calories from carbs (488g) had an RQ of 0.83 (R). So if you eat 222g of protein and 488g of carbs (close to 1:2 ratio), your RQ will not reach very high. But you do drop protein to 150g while keeping carbs the same, your RQ will most likely increase.
Can you burn and lose fat on a low fat diet?
The answer is yes.
We’re always burning a certain amount of fat at all times. We always burn fat, but at different degrees. For example, burning carbs blocks fat oxidation by more than 90%. So there is still a small amount of fat oxidation going on even after consuming massive amounts of carbs.
And glucose oxidation only inhibits the transport of long chain fats into the mitochondria and not medium or short chain fats. So if you have some coconut oil or MCT oil with your carbs, your body will born those alongside the carbs.
“For high-carbohydrate diets, the RQ is lower than is the FQ, indicating that subjects must mobilize body fat. This is supported by data on body weight loss in subjects changing from a standard maintenance diet to a low-fat diet, even while energy intake was increased with nearly 20%.” (R)
Eating more carbs at the expense of fats, especially if it’s a combination of glucose and fructose, such as honey and fruit, will speed up the metabolic rate so that you can eat more while maintaining the same weight.
And even beneficial metabolic boosters, such as caffeine, thyroid, androgens, etc., promote the oxidation of fat. But more on the in a bit.
From the study above (R), a high carb diet results in more fat loss, at least in the first 6 days.
How do we boost the metabolic rate?
Thyroid, androgens and various foods are able to boost the metabolic rate. Some people might think that muscle mass contributes the most to metabolic rate, but it’s actually our organs.
“Most of the overall RMR (∼60%) arises from four organs: liver, kidney, heart and brain, although they represent only ∼5% of body weight (Table 3).9 Their metabolic rates are 15–40 times greater than that of the equivalent weight of muscle mass (∼10–15 kcal/kg/day) and 50–100 times greater than that of adipose tissue (∼4.5 kcal/kg/day).” (R)
Androgens promote the size of our organs, whereas stress hormone decrease their size.
Thyroid boosts the metabolic rate of these organs, thus further enhancing the metabolic rate.
Thyroid, metabolic rate and fat oxidation
For those that are afraid of fat oxidation, thyroid, one of our main drivers of health, boosts fat oxidation.
Hyperthyroidism and RQ
For example, people with Grave’s disease burn a lot more fat than those that are euthyroid. Once they go for treatment to bring their thyroid function to normal, their fat oxidation drops down and their RQ increases.
This study showed a reduction in metabolic rate, fat oxidation and resting energy expenditure (28.7 ± 4.0 kcal/kg to 21.5 ± 4.1 kcal/kg) and an increase in respiratory quotient (from 0.76 to 0.81) (R).
Thyroid and metabolic rate
But we don’t want to be hyperthyroid, nor hypothyroid. Thyroid hormones correlate with the metabolic rate, so if we want to lose weight, we want to have optimal thyroid hormone production and conversion. Metabolic rate is inversely correlated with TSH and positively with T3. But don’t just look at TSH, because TSH might actually be normal, but then T3 can still be low.
“Although the study population was heterogeneous, including patients with hypothyroid with different etiologies, and the EE (energy expenditure) recording was limited to REE (resting energy expenditure), it suggests that normalization of TSH may not equate to a state of euthyroidism as it relates to energy metabolism and that a state of tissue hypothyroidism may contribute to a decrease in EE.” (R).
On average, resting metabolic rate (RMR) accounts for about 60–70% of TEE (total energy expenditure), the remainder being accounted for by diet-induced thermogenesis (10%) and physical activity (∼20–30%). But spontaneous energy expenditure (SEE) can be much higher, depending on your energy levels. SEE can be as high as 2000 calories per day. Thyroid hormones promote energy production which then promotes movement, such as fidgeting, walking around more, moving your arms more, etc., and that all adds up. So although thyroid hormones themselves don’t necessarily boost the metabolic rate by all that much, but by enhancing your energy, it can make you be more active and lose more weight.
But the key here is that thyroid doesn’t stimulate only fat oxidation, but glucose oxidation as well.
“In rat skeletal muscle T3 rapidly activates the protein kinase B (PKB)/Akt pathway, resulting in the stimulation of both fatty acid and glucose metabolism.” (R) That’s what we want.
Where should our thyroid hormone be at?
TSH at or below 1 and fT3 at around 5pmol/L.
This study found that mean fT3 was 3.9 ± 0.1 pmol/L (3.1-6.8) in obese subjects compared to 5.0 ± 0.1 pmol/L in non-obese controls, respectively, however, fT4 was similar in the 2 groups (R). So even a 1 pmol/L can make a big difference over a long period of time.
But it’s not necessarily the fT3 that matters, but the tissue levels of T3. How well are T3 taken up by tissue and how well do they activate the thyroid hormone receptors. Many things can inhibit proper thyroid hormone uptake and activation. Things like inflammation, endotoxin, polyunsaturated fat, endocrine-disrupting chemicals, stress hormones, etc.
And this is where aspirin comes in. If you have tried thyroid and it just hasn’t worked all that well, then try some aspirin either with or without thyroid. Aspirin lowers stress hormones, excess free fatty acids, inflammatory mediators, etc., and enhances thyroid hormone uptake into a cell. It has many other metabolic boosting benefits as well and most people that I have recommended thyroid to have responded positively to in terms of sleep, energy, mood, temperature, etc.
Testosterone, DHT, metabolic rate, RQ and fat loss
Hypogonadism or low testosterone is associated with weight gain and diabetes. Giving men testosterone or DHT can help to reverse this.
And testosterone and DHT enhances the metabolism of both fat and glucose.
“Testosterone optimizes fat oxidation vs hypogonadel men.” (R)
The study below shows that testosterone reduces glucose oxidation, but in the case of mitochondrial damage and diabetes, glycolysis is significantly upregulated, which leads to glucose wasting. So the body thinks there is a glucose deficiency, which then upregulates glucose production in the liver and more glucose wasting to lactate. In that case, testosterone can inhibit the wasting of glucose.
“Basal lipid oxidation (b = 5.65 mg/min/m2, p = 0.045) increased and basal glucose oxidation (b = −9.71 mg/min/m2, p = 0.046) decreased in response to testosterone therapy even when corrected for changes in LBM.” (R)
Some people might think that the insulin-sensitizing effects of testosterone are due to either testosterone or estrogen, but blocking 5AR, thus lowering DHT, prevents the beneficial effects of testosterone.
“However, 8-week resistance training in OLETF rats significantly increased the levels of muscle sex steroid hormones and protein expression of steroidogenic enzymes with a concomitant increase in skeletal muscle mass, improved fasting glucose level, and insulin sensitivity index. Moreover, resistance training accelerated glucose transporter-4 (GLUT-4) translocation and protein kinase B and C-ζ/λ phosphorylation. Administering the 5α-reductase inhibitor in resistance-trained OLETF rats resulted in suppression of the exercise-induced effects on skeletal muscle mass, fasting glucose level, insulin sensitivity index, and GLUT-4 signaling, with a decline in muscular DHT levels. These findings suggest that resistance training-induced elevation of muscular DHT levels may contribute to improvement of hyperglycemia and skeletal muscle hypertrophy in type 2 diabetic rats.” (R)
So DHT helps the body use glucose correctly.
This study found that DHT increased the RQ.
“DHT decreased the oxygen consumption (VO2), whereas it did not have any significant effect on the CO2 produced (VCO2; Figure 4 A and B). The decrease in VO2 but not in VCO2 resulted in an increased RQ (Figure 4C). Furthermore, when calculating fat and glucose oxidation, it was shown that DHT treatment resulted in a decreased fat oxidation, whereas glucose oxidation was increased.” (R)
How many carbs do I need?
This study (R) shows that cortisol levels are much higher at 140g carbs per day vs 352g at a 30% deficit. So if you want to go into a big deficit, then 60-70% of your total calories from carbs will be the best to protect against the stress. If the deficit is smaller, then less can be eaten, but it’s not necessary to eat less, since a smaller deficit and high carb intake will create a higher RQ. More CO2 for more health benefits.
Since we want to have a higher RQ, we’ll have to eat high carb.
De novo lipogenesis (DNL) is the synthesis of new fat from carbohydrates. Some people are concerned that eating high amounts of carbs, especially fructose will cause excess fat synthesis and fatty liver, etc.
This study found that fractional DNL increased more than 10 fold when a surplus of carbohydrates was consumed. However, despite a 10 fold increase, absolute DNL accounted for less than 5g of fatty acids synthesized per day even on a +50% surplus from carbohydrates (R). And when you go into a deficit, DNL is reduced. Studies show that carb oxidation equals carb intake. No matter if it’s 200g or 600g per day. And this is because there is limited storage space for carbs. The body burns it rather than converting it.
The amount of energy stored in the form of fat is large, representing 92–98% of all endogenously stored energy, whereas carbs only contribute to about 2–8% (R). So it’s much more important to focus on reducing fat intake rather than carb intake if the goal is to lose weight.
Should you rely only on glucuronidation for fat loss?
Another reason for avoiding a big deficit is so that the body is not flooded with PUFAs from enhanced lipolysis. The goal is to have your liver detox these fats, through glucuronidation instead of using them as fuel.
Glucuronidation, more correctly glucuronosylation, is the addition of glucuronic acid to a substrate. Glucuronidation is often involved in xenobiotic metabolism of substances such as drugs, pollutants, bilirubin, androgens, estrogens, mineralocorticoids, glucocorticoids, fatty acid derivatives, retinoids, and bile acids.
Certain glucuronidation enzymes in the liver, namely UGT1A and UGT2B families, are to convert PUFA and their metabolites into glucuronide derivatives, which is considered an irreversible step to inactivation and elimination of endogenous substances from the body (R).
So we want these enzymes to be in tip-top shape to maximize the detoxification of toxins. But it’s not just the PUFAs we should be worried about, but also all the other toxins that are stored in the fat as well.
We don’t know how many grams of PUFA and PUFA metabolites are detoxed by these enzymes per day and that will also differ greatly between each individual. So to try to determine the amount of PUFA coming in from the diet and the amount of PUFA released from the adipose stores and its relation with the ability of the UGT enzymes to detox them is ludicrous.
That will create unnecessary stress and stress is anti-metabolic.
How to enhance PUFA detoxification
A few foods and substances that enhance this pathway (UGT enzymes) include cruciferous vegetables, citrus foods, dandelion, rooibos tea, honeybush tea, rosemary, ellagic acid, ferulic acid, curcumin, astaxanthin, ferulic acid, etc.
Foods that supply the D-glucaric acid for the UGT enzymes include: mung bean seeds, adzuki bean sprouts, oranges, spinach, apples, carrots, alfalfa sprouts, cabbage, Brussel sprouts, cauliflower, broccoli, grapefruit, grapes, peaches, plums, lemons, apricots, sweet cherries, corn, cucumber, lettuce, celery, green pepper, tomato, potato, etc.
After glucuronidation has added a glucaric acid, it’s ready for detoxification, but there is also an enzyme, beta-glucuronidase, that reverses the UGT conjugation reactions and preventing detoxification. Inflamed tissue contains high amounts of this enzyme so lowering inflammation would be key to keeping this enzyme low. Other things that lower the activity of this enzyme are saturated fat (polyunsaturated fat promotes this enzyme) and proanthocyanidins rich foods, such as strawberries, blackcurrant, cocoa, calcium, magnesium, vitamin C, Gotu Kola, etc. And last, but not least, my favorite for this, cardamom spice.
Nuclear factor (erythroid-derived 2)-like 2, also known as Nrf2, is a transcription factor that increases the promotes the activity of phase II detoxification and antioxidant enzyme genes in the body. In vivo (meaning studies done in living beings, such as humans and animals) evidence shows curcumin, broccoli constituents, garlic, epicatechins, ginger, purple sweet potato, isoflavones, coffee, rosemary, pomegranate, naringenin, ellagic acid, astaxanthin, γ-tocopherol, chlorophyll, blueberries and EGCG promote Nrf2 activity, and thus promote phase II detoxification (R).
You might feel a little overwhelmed with all the food options listed above, but if you can just have citrus, pomegranates (and just fruit in general) and coffee, that will take you far.
Bile acids that activate FXR induces intestinal UGT1A1 (R).
Glucose induce UGT1A1 (R).
Calcium-d-glucarate can provide glucaric acid. 200mg once or twice a week can be helpful.
- Fat oxidation is inevitable and isn’t bad. Excess fat oxidation at the expense of glucose oxidation is bad.
- Moderate carb isn’t bad, but going too low can increase cortisol and lower thyroid hormones. High carb diets help to optimize T3 levels and minimize cortisol.
- Keeping your carb intake at >60% of total calories is a good way of keeping your RQ high.
- Eating too much protein can lower RQ, but protein is still needed for thermogenesis and satiety. Between 15-20% is a good number to shoot for. Or simply 100-120g protein from meat, eggs and dairy and 30-50g from gelatin.
- Try to get a large amount of your carbs from honey, maple syrup and/or fruits.
- Go into a small deficit of 5-10% to minimize a drop in RQ and prevent cortisol from increasing too much.
- Make sure your thyroid hormones are in a good place before attempting a deficit.
- Preferably have your TSH at or below 1 and your fT3 at around 5 pmol/L.
- If your fT3 is low, then selenium and iron might be too low. Glucose is also needed for thyroid hormone conversion.
- Do high-intensity exercise, such as sprinting, as that upregulates glucose oxidation pathways, increases the metabolic rate, boosts testosterone and DHT production and improves insulin sensitivity. But don’t do it too frequently or intensely or that can also be too taxing.
- Optimize liver function with protein and fruit and honey consumption. Drink milk or eat dairy as the calcium can help to neutralize the toxicity of PUFAs (R).
- Use 1tsp cardamom once daily if your gut is inflammatory to support proper detoxification of toxins.
- Consume 1 tsp coconut oil in the morning. Coconut oil has similar properties to vitamin E and can protect against the harmful effects of PUFAs.
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