Can the 16:8 Intermittent Fasting Method Help You Lose Weight?
The Science Behind [16+8]: Intermittent Fasting
First, the conclusion: It is feasible!
The 16+8 weight loss method involves eating all three meals within an 8-hour window, followed by 16 hours of only water consumption, with no food intake.
As early as 2022, Humaira Jamshed and colleagues published a randomized clinical trial in JAMA Internal Medicine, finding that early time-restricted eating (eTRE), which involves eating during an 8-hour window from 7:00 AM to 3:00 PM while following a low-calorie diet (500 kcal/d below resting energy expenditure) and exercising 75 to 150 minutes per week for 14 weeks, effectively resulted in a weight loss of 6.3 kg, and even improved diastolic blood pressure and mood disorders [1].
1. Participants (90 Individuals)
2. Grouping
3. Other Conditions
4. Results
The experimental group (eTRE+ER) lost an average of 6.3 kg, while the control group (CON+ER) lost 4.0 kg. Additionally, the eTRE+ER group experienced greater improvements in mood, including reductions in fatigue, increased vitality, and decreased feelings of depression/dysphoria. However, there were no statistically significant differences between the two groups in terms of absolute fat reduction or the ratio of fat loss to weight loss.
It is evident that both the control group and the experimental group showed a decrease in weight, indicating that simply restricting diet and maintaining exercise can lead to weight loss over time. However, combining this with the [16+8] intermittent fasting approach can yield even greater weight loss results!
Of course, aside from [16+8], let’s take this opportunity to explore what else scientists have discovered about weight loss!
Timing: Early Breakfast and Dinner (8~9 AM)
Research has indicated that implementing time-restricted eating (TRE), which involves extending the overnight fasting period to over 12 hours, may be associated with improvements in several key cardiovascular health indicators [2]. Thus, fasting methods should be as scientifically sound as possible!
Anna Palomar-Cros and colleagues found that eating the first meal later (after 9 AM) and the last meal earlier (before 8 PM) is associated with a higher cardiovascular risk, particularly in women. In contrast, adopting (1) an earlier eating pattern, meaning having breakfast and dinner earlier; (2) a longer overnight fasting period; and (3) fasting without skipping breakfast may have potential benefits for preventing cardiovascular diseases [2].
Details of the study are not elaborated here; interested readers can refer to the original research.
Principle: Cutting Out Carbs? No!
Staple foods are still essential! However, researchers have found that supplementing with resistant starch can promote weight loss.
Resistant starch (RS), also known as resistant digestible starch or indigestible starch, refers to a type of fermentable dietary fiber that cannot be digested by human amylase in the small intestine and instead enters the colon, where it is fermented by the gut microbiota. RS is found in most natural foods, such as potatoes, bananas, and rice.
In February 2024, Huating Li and colleagues published a study in Nature Metabolism [3]. An 8-week RS intervention for overweight individuals helped achieve an average weight loss of 2.8 kg, with significant reductions in fat mass and waist circumference starting from the second week of RS supplementation (Fig. 3).
1. Participants (90 Individuals)
Obese/Overweight Individuals: Ages 18-55, with a body mass index (BMI) ≥ 24 kg/m² and/or increased waist circumference (men ≥ 85 cm, women ≥ 80 cm). None had chronic diseases, were undergoing treatment affecting glucose metabolism, or had recently used antibiotics or probiotics (within the last three weeks).
2. Trial Design
The study consisted of alternating consumption of resistant starch (RS) derived from corn or energy-matched control starch (CS) over two 8-week periods, with a 4-week washout period between the two cycles. The total study duration was 20 weeks, including two 8-week intervention phases, where participants were randomly assigned to two groups: (1) RS-Washout-CS or (2) CS-Washout-RS. Data from after the RS intervention were compared with data after the CS intervention.
Starch was provided in powdered form, packaged in ready-to-eat sachets, to be mixed with 300 mL of water. Participants were instructed to consume one sachet 10-15 minutes before meals, twice daily.
Other Conditions
Participants followed a standardized background diet, categorized as either lightly active or sedentary. Based on ideal body weight (Ideal Weight (kg) = Height (cm) - 105), a daily intake of 25 kcal/kg was provided, with macronutrient distribution of carbohydrates (50-60%), fats (25-30%), and proteins (15-20%). Participants were allowed one fruit per day and were advised to avoid high-sugar beverages and snacks.
Results
The experimental group experienced an average weight loss of 2.8 kg after the RS intervention, while no significant changes were observed in the control group after the CS intervention.
Compared to the CS intervention, the RS intervention led to significant reductions in fat mass and waist circumference. During the RS intervention, participants' weight, waist circumference, and fat mass began to decline significantly from the second week onwards. Additionally, after the RS intervention, the visceral fat area and subcutaneous fat area measured by abdominal MRI were both lower than after the CS intervention.
Furthermore, the RS intervention also improved insulin resistance (as obesity significantly leads to complications such as diabetes and cardiovascular diseases). Researchers found that RS primarily affects and improves changes in the gut microbiota composition in the body, particularly with a significant increase in the number of Bifidobacterium adolescentis (B. adolescentis). The RS-induced changes in gut microbiota increase the secretion of secondary bile acids, reduce inflammation by restoring the gut barrier, and inhibit lipid absorption, thereby facilitating weight loss [3].
Unlocking What You Don’t Know About Obesity
Obesity is more importantly associated with health issues related to many serious diseases! The most common complications include fatty liver, diabetes, dyslipidemia, and hypertension. Obesity is actually considered a state of chronic low-grade inflammation, indicating that obesity is not as simple as we might think!
Obesity: A Chronic Inflammation
A body mass index (BMI) over 25 is considered overweight, while a BMI over 30 is classified as obesity. Overweight and obesity are defined as abnormal or excessive fat accumulation that poses a risk to health.
Currently, adipose tissue is no longer viewed as a passive energy storage depot; it is recognized as a complex endocrine and immune organ that actively secretes many bioactive substances. Yes, that’s right! Adipose tissue is an organ!
In addition to classic white adipose tissue (WAT) and brown adipose tissue, adipose tissue contains a large number of immune cells. Furthermore, adipose tissue exhibits site specificity, high plasticity, and heterogeneity, playing a crucial role in maintaining the body's energy homeostasis [4].
In obesity, the composition of WAT undergoes significant dynamic changes in cellular morphology and phenotype, causing adipocytes to expand to their limits, ultimately leading to cell death and inflammation [5]. A hallmark of immune dysregulation caused by obesity is the increased abundance and diversity of lipid-associated macrophages (LAMs) in WAT. In obesity, persistent inflammation of adipose tissue (AT) creates a form of cellular memory that limits the effectiveness of weight loss interventions. This means that weight loss induced by dietary and/or lifestyle interventions does not consistently reverse the adverse inflammatory responses associated with obesity in adipose tissue.
Overall, pro-inflammatory immune cells dominate early obesity, while resident anti-inflammatory adipose tissue macrophages (ATM) prevail in chronic obesity. Some of these anti-inflammatory ATMs are transcriptionally intermediate between monocytes and mature lipid-associated macrophages (LAM), consistent with pre-LAM. Pre-LAM are spatially associated with crown-like structures (CLS) in early obesity, indicating adipose tissue dysfunction.
Spatial data show the co-localization of ligand-receptor transcripts related to lipid signaling between monocytes, pre-LAM, and LAM, including Apoe, Lrp1, Lpl, and App. The expression of these ligands in pre-LAM during early obesity suggests signaling to LAM within the CLS microenvironment.
p53 Signaling Regulates the Effects of Intermittent Fasting
Early studies on obese mouse models indicated that the transcription factor p53 is involved in regulating adipocyte stress responses, which may signal the recruitment of macrophages [6].
Recent research published in Nature Communications further discovered that p53 signaling in adipocytes determines the accumulation of lipid-associated macrophages (LAM) in the visceral adipose tissue of obese mice under intermittent fasting (IF) and regulates the fasting effects in both mice and humans [6].
In the context of obesity, intermittent fasting increases the abundance of LAM in the crown-like structures of visceral adipose tissue in mice. The increase in LAM abundance is strongly dependent on p53 and is partially mediated by p53-driven adipocyte apoptosis.
Specific knockout (KO) of p53 in adipocytes can prevent the accumulation of LAM during IF, reduce inflammation and apoptotic signaling, while enhancing the catabolic state of adipocytes and improving systemic metabolic flexibility and insulin sensitivity.
Therefore, p53 KO leads to weight loss and enhances the metabolic health benefits of intermittent fasting.
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