This statement summarizes the general conclusion reached by a recent Cochrane review published in 2026. The review, in a meta-analysis combining data from 22 randomized controlled trials examining intermittent fasting approaches in overweight or obese adults, reported that intermittent fasting did not demonstrate a significant advantage in terms of weight loss compared to standard dietary approaches with similar calorie intake (Garegnani et al., 2026). However, making generalizations like "intermittent fasting doesn't work" is easy but scientifically incomplete. Such analyses often assess the magnitude of weight loss and average effects; practically important details such as who found which method more sustainable, which behavioral model was easier to implement, and potential metabolic effects beyond weight loss may not be answered with the same clarity. Therefore, let's evaluate this result more closely and within a more accurate context.

In the studies included in this meta-analysis, when total calorie intake was equalized, individuals practicing intermittent fasting and those following standard dietary recommendations lost similar amounts of weight. In other words, both approaches were more effective than doing nothing. This is to be expected, as the main factor determining weight loss is energy balance. Whether a calorie deficit is achieved through meals spread throughout the day or at specific times is secondary.

In clinical practice, what matters is not just this theoretical equivalence, but the sustainability of the method. For many, calorie counting is a challenging approach that eventually leads to abandonment. Intermittent fasting, on the other hand, offers a simpler rule, such as not eating during certain hours of the day. Therefore, for some individuals, achieving a calorie deficit can become more natural and sustainable in the long term. So, in practice, for some people, the real comparison is not between intermittent fasting and a classic diet, but between intermittent fasting and doing nothing. This is because these individuals may have previously tried calorie counting, portion control, or consistently following diet rules but failed to sustain them. In this case, a single, clear rule, such as not eating during certain hours of the day, can make behavioral change much easier.

The mechanism here is actually simple: when a person skips breakfast or eats dinner early and then doesn't eat anything afterward, their total daily calorie intake unconsciously decreases. It becomes easier to create a calorie deficit simply by shortening the time window, without needing to constantly calculate what they eat throughout the day. This makes the method particularly applicable for people with busy lifestyles or those who don't want to constantly monitor their diet.

Therefore, for some individuals, intermittent fasting, even if theoretically appearing “equal” to other diets, may become the only viable option in practice. Thus, the realistic question for that person is not “intermittent fasting or a conventional diet?” but rather “intermittent fasting or yet another unsustainable diet experiment?” This distinction is often overlooked when interpreting clinical outcomes, but it is quite important from a behavioral science perspective.

At the same time, intermittent fasting is not a method used solely for weight loss. Therefore, limiting its effects only to changes on the scale would not be an accurate approach. The rhythmic alternation of fasting and eating periods affects a range of physiological systems, from metabolic flexibility and circadian timing to glucose regulation and sleep patterns.

When we consume food frequently throughout the day, our bodies remain primarily in a 'glucose-dependent' energy utilization model. When a person eats at frequent intervals throughout the day, blood sugar levels rise each time. In response, the pancreas releases the hormone insulin. The main function of insulin is to transport glucose from the blood into cells and store excess energy. Therefore, insulin levels often don't have the opportunity to fully decrease in people who eat frequently throughout the day.

When insulin levels are high, the body is reluctant to use its stored fat. This is because insulin also acts as a "storage signal," halting fat burning. The release of fatty acids from fat cells into the bloodstream, or lipolysis, is suppressed. In this state, the organism primarily meets its energy needs from glucose in the blood and glycogen stored in the liver and muscles. In other words, the body constantly uses "newly arrived sugar" and short-term carbohydrate stores as fuel.

This can be explained with a simple analogy: Imagine you have both a refrigerator and a freezer at home. If you constantly buy fresh food from the market and fill the refrigerator, you'll never touch the stores in the freezer. The body's response to frequent eating is similar. Glucose and glycogen stores in the blood are used, while fat stores remain in reserve.

When meal intervals lengthen and insulin levels drop, the situation changes. Fresh food in the refrigerator decreases, and the body begins to use energy stored in fat tissue. Lipolysis kicks in, fatty acids are released into the bloodstream, and energy production becomes increasingly fat-based. A significant portion of the metabolic effects of intermittent fasting is related to this fuel shift. When food intake is cut off, i.e., when fasting periods are extended, metabolism gradually shifts to a different fuel strategy. Glycogen stores in the liver decrease, free fatty acids are mobilized from fat tissue, and hepatic ketogenesis increases. Thus, ketone bodies begin to be used as an alternative energy substrate in many tissues, including the brain. This shift is an indicator of the capacity defined as "metabolic plasticity" and is closely related to metabolic health (Goodpaster and Sparks, 2017).

Metabolic plasticity refers to an organism's ability to fluidly switch its fuel source according to its energy needs and nutritional status. Efficient glucose utilization in the post-meal period and the seamless transition to fatty acids and ketones during fasting are key indicators of this plasticity. Frequent eating and snacking throughout the day can contribute to the gradual decline of this plasticity. Over time, the organism becomes slower and less efficient in its transition to fat burning during fasting. Experimental studies show that frequent feeding and a constant energy surplus impair the ability of muscles and the liver to convert fat, while longer intervals between meals or periods of energy restriction can restore metabolic plasticity (Kelley and Mandarino, 2000; Goodpaster and Sparks, 2017; Longo and Panda, 2016).

It is also important to know that this fuel shift is not simply a change in energy source. That is, when fasting periods are prolonged, we are not just talking about more effective fat burning. With the decrease in nutrient signals, cellular adaptation mechanisms such as AMPK activation, mTOR suppression, and sirtuin pathway stimulation are activated. This environment also supports autophagy processes, where damaged proteins and organelles are recycled within the cell. Autophagy is a fundamental maintenance mechanism that provides cellular quality control and increases during periods of energy restriction or fasting, and plays a central role in the biology of neurodegenerative diseases and aging (Mizushima and Komatsu, 2011; Longo and Mattson, 2014). It has been observed that these cycles are less activated in modern diets dominated by constant nutrient abundance, while intermittent fasting periods can reactivate these repair processes. In this area, the work of Mark Mattson and his team, in particular, shows that intermittent fasting is associated with more significant improvements in some cognitive performance measures compared to the standard healthy eating pattern, and that this may be linked to a unique "starvation physiology" (Mattson et al., 2018).

From a brain perspective, the use of ketone bodies does more than just provide alternative fuel. Ketone metabolism is associated with increased mitochondrial efficiency, reduced oxidative stress load, and increased neurotrophic factors such as BDNF. Experimental and clinical studies show that intermittent energy restriction can support synaptic plasticity and neuronal resilience (Mattson et al., 2018). Therefore, some cognitive effects of intermittent fasting are thought to be related to the transition from a glucose-dependent continuous feeding state to a fat and ketone-based intermittent feeding state, rather than solely due to weight loss.

In conclusion, intermittent fasting makes it possible to shift the organism from a glucose-dependent, constantly nourished metabolic mode throughout the day to an alternative mode that utilizes stored energy and where autophagy and cellular repair processes are more active. This physiological shift can be significant not only for weight control but also for metabolic flexibility and neurological resilience. Therefore, evaluating intermittent fasting solely based on the question of "how much weight does it help lose" would be to unnecessarily narrow the biological scope of the method.

Many people, myself included, observe significant benefits when practicing intermittent fasting or time-restricted eating. More stable energy levels in the morning and improved sleep patterns at night are generally the most common benefits. The physiological basis for this is understandable: food intake in the early hours of the day coincides with a period of higher insulin sensitivity, while eating late in the day more easily disrupts glucose regulation and the circadian rhythm, negatively impacting sleep quality. The literature increasingly demonstrates that properly timed eating windows are associated with metabolic health, circadian alignment, and neuronal resilience mechanisms (Longo and Panda, 2016; Mattson et al., 2018).

Of course, intermittent fasting isn't always advantageous. Especially for those who train intensely, long periods of fasting or very narrow eating windows can lead to insufficient total energy intake; this can result in decreased performance, difficulty recovering, and short-term energy depletion. Therefore, these individuals need to pay particular attention to protein intake.

In short, it's not accurate to classify intermittent fasting as absolutely "good" or "bad." Its effectiveness varies depending on the context, the individual, lifestyle, and goals. Therefore, when encountering headlines like "intermittent fasting doesn't work," the real question to ask is: why doesn't it work? In terms of weight loss, metabolic health, sleep, or cognitive function? Often, making this distinction is more revealing than the overall conclusion of a single study or meta-analysis.

I wish you healthy days,

Dr. Ahmet Ozyigit
Elite Research and Surgical Hospital