Midlife is full of change. Families shift with parents aging and kids growing, eventually leaving the nest. Careers build and transition. Relationships ebb and flow. And that’s just the external atmosphere. Internally, hormones can wreak havoc on our bodies and minds. It’s called a second adolescence for good reason.
Estrogen, insulin, cortisol, leptin and ghrelin are 5 of the hormones that contribute to the insidious expansion of our middles during midlife. The following sections detail the “how” of each hormone and give you steps to take to beat them at their own game.
Starting in peri-menopause (5-10 years prior to menopause), the female sex hormones, progesterone and estrogen, which used to work in perfect harmony, start to dwindle and disengage from each other leading to relative excesses and insufficiencies.
Estrogen excesses (relative to progesterone levels) can be responsible for, among other things, irregular periods (especially excessive vaginal bleeding), bloating, and mood swings (bouts of depression).
A hallmark of menopause (besides the defining: no period for 12 months) is estrogen decline. And that’s the main cause of many potential symptoms menopausal women face including hot flashes, night sweats, vaginal dryness, mood swings, mental fuzziness and changes in libido.
In pre- and peri-menopasual women, ovaries are the primary site of estrogen production. Not so in post-menopausal women when the ovaries no longer produce estrogen. Instead, after menopause the primary location of estrogen production is fat cells (adipocytes).
FYI: It turns out the increased risk for breast, endometrial and ovarian cancers in obese postmenopausal women comes from the increased estrogen in the system that is promoted by the extra fat cells. Good news: losing the fat can decrease the risk.
ESTROGEN AND FAT
Estrogen decline does not lead to weight gain, it leads to fat redistribution.
There was no consistent information, nor clear evidence that showed that estrogen decline directly causes weight gain.
There can definitely be weight gains during midlife so the assumption seemed fair. But the mechanism is more complicated than: decreased estrogen = increased weight.
What does seem to happen with estrogen decline is fat redistribution with more fat in the abdomen than before menopause.
This is the case even if there is no change in weight.
It appears that the new ratio of estrogen to testosterone is responsible for this development—turning women’s bodies from pear-shaped to apple-shaped—more like men’s (our risk for heart disease increases to that of men’s with this change as well).
Abdominal fat can lead to insulin resistance (see insulin section), which can further increase abdominal fat stores. A cycle we want to avoid.
The good news is that aerobic exercise (even walking) preferentially reduces abdominal fat. So starting and keeping a weekly exercise regimen will go a long way to preventing and/or mitigating estrogen induced fat redistribution.
Insulin’s vital to life. It’s first job is to direct glucose into cells because glucose can’t do that on it’s own. Glucose, which is the primary fuel for cells, comes from the carbohydrates we eat. Without insulin, cells (read: we) would die.
Insulin is also known as the fat storage hormone.
And when we are talking about weight gain or loss, we must remember to think of it this way.
It works like this: insulin shunts glucose into the cells for immediate use until they’ve reached their limit and then insulin helps store the extra glucose as glycogen for future use.
This storage happens primarily in liver cells (hepatocytes) and once the glycogen reserves are topped off, the liver starts storing the excess fuel as fat.
If there continues to be lots of excess fuel (glucose from carbohydrates) insulin facilitates the fat storage and you get weight gain, fatty liver and eventually obesity.
INSULIN AND FAT: INSULIN RESISTANCE
Insulin resistance is like pouring gasoline on the weight gain fire. If someone has insulin resistance, their insulin isn’t well recognized by their cells. So insulin can’t get it’s normal job of getting glucose into cells done efficiently.
The pancreas (the organ that makes insulin) tries to remedy the situation by producing more insulin. Then we are left with high levels of both glucose and insulin in the bloodstream, which leads to rampant fat storage (particularly abdominal fat).
Medical researchers are not sure what causes insulin resistance, but they have established a link between abdominal fat and insulin resistance, even in normal weighted people.
Abdominal fat, also known as visceral fat, accumulates in and around your organs and is associated with inflammation, which can lead to diabetes, cardiovascular disease, stroke and death. It’s bad. And should be avoided at all costs.
Even those of us without insulin resistance can have an increased baseline insulin level that leads to (abdominal) fat storage.
Here’s how: The Standard American Diet is high in processed sugar and flour and often involves overly large portions of food. These two factors increase our baseline insulin levels by providing an immediate and excessive amount of glucose from the big portions of refined carbohydrates. Then large doses of insulin are released to compensate for the glucose. The excesses set us up for (abdominal) fat storage.
Carbohydrates mixed with water and fiber (like in vegetables) aren’t as readily available and do not trigger the same magnitude of glucose-insulin response.
Focusing on veggies and limiting processed foods with refined sugar and flour allows for a normal glucose-insulin response that uses the fuel for immediate energy and not fat storage.
Cortisol is one of the hormones released by the adrenal gland in response to the brain’s signal that there’s a perceived eminent threat. At it’s best, it is episodic, only released when there’s potentially fatal danger. In a safe environment that’s likely a rare event.
But if we’re used to thinking of that work deadline as a life-or-death situation, we could be experiencing “threats” all day long.
The problem is that the system was not designed for on-going, chronic stress like this. Your body can handle the disruptive effects of cortisol in small doses with time for full recovery in between. But, there are negative consequences if the alarm bell’s ringing all the time.
CORTISOL AND FAT
Cortisol excesses contribute to weight gain by releasing glucose in the bloodstream, increasing sugar cravings, and fostering overeating to calm the system.
In order to prepare your body to deal with danger, cortisol ramps up some key functions and suppresses other non-essential ones.
The one we’re most interested in here is the increase in availability of glucose in the blood. Cortisol does this to fuel the places that need it most during a crisis, your brain and muscles.
This is great for short-term bursts of energy but not great on a continual basis. In fact, if it’s happening all the time, you gain weight.
Remember our friend insulin? When there’s a steady stream of extra glucose floating around you release insulin to deal with it. Your baseline insulin level is therefore elevated which leads to fat storage, particularly in the abdominal area.
The targeted release of insulin to deal with the excess stress glucose can also lead to food cravings by creating a “crash” and subsequent desire for sugar.
Unrelenting stress causes cravings in another way, too. Your body attempts to calm your amped up system by using the habituated reward pathways in the brain. For many of us that includes high fat, high sugar foods. Powerful cravings for “comfort foods” and overeating lead to weight gain, often rapid, in response to chronic stress.
Frustration over a congested email inbox isn’t the only thing that may raise your cortisol level. Sleep deprivation, intense exercise and caffeine increase it as well.
Lifestyle changes go a long way to even out your hormones.
Moderate exercise like walking, preferably in nature, gives you the health benefits of exercise without raising your stress hormone levels.
Deep breathing, yoga, meditation, relaxing music and massage all decrease your cortisol.
Laughter and joy lower it, too. As does interacting with your pet, prayer and acts of kindness.
Creating a calm, fulfilling life protects you.
Leptin is the hormone responsible for telling our brain to stop eating and get active.
Leptin is produced primarily in fat cells (adipocytes), which makes sense: more fat should tell your body to stop eating and get active. And that feedback loop does work, except when it’s blocked.
LEPTIN AND FAT: LEPTIN RESISTANCE
Leptin resistance is similar to insulin resistance in that there’s enough circulating hormone, it just doesn’t function normally at its site of action.
Leptin resistance seems to occur once overeating leads to overweight and obesity. So high levels of leptin are found in obese people instead of the expected lower levels.
How overeating and obesity leads to leptin resistance is not completely understood yet but our buddy, insulin has been implicated. Both insulin and leptin act on similar cells in the brain and it has been established that in obesity, insulin levels are increased. Now we know leptin levels are too.
But which comes first: fat, insulin or leptin?
We do know that lowering insulin levels will increase leptin sensitivity, meaning the circulating leptin will work better.
Insulin levels decrease with weight loss. So losing weight leads to increased leptin sensitivity and lower circulating insulin levels. Creating a positive weight loss cycle.
Ghrelin is the hormone that tells us we’re hungry. It’s a fast-acting hormone that increases appetite.
It’s released in the stomach and communicates with the brain. When it’s working normally, there’s more released before meals when the stomach is empty and less after them, when it’s full.
Additionally, as ghrelin increases, it indirectly blocks leptin in the brain thereby increasing the likelihood of feeding.
All this is normal. It’s the way our bodies maintain their energy stores, signaling health and a safe environment full of fuel.
GHRELIN AND FAT
Overeating and obesity disrupt these normal appetite mechanisms creating a vicious cycle of weight gain.
We’ve all been there; we keep eating because it tastes so good, even though we’re full. If we continue to do this day in and day out we disable our appetite regulators.
Hormone sensitivities change with weight gain. One can become leptin resistant and more sensitive to ghrelin when obese. To make matters worse, as obese people lose weight their ghrelin may increase in an attempt to keep the status quo. This is not permanent, however, and mechanisms can return to normal when a new balance is reached.
You don’t have to be obese to increase your ghrelin response. If we are sleep deprived, eat a high fat diet or experience excessive stress we get hungrier thanks to more ghrelin.
Higher protein, high fiber meals suppress ghrelin release because protein and fiber are processed more slowly than refined carbohydrates in our stomach. We remain fuller longer thereby delaying the usual release of ghrelin.
So get good sleep, manage stress and eat lower fat, higher protein and fiber meals to better regulate your hunger hormones.
There you have it. A review of five hormones and how they can contribute to weight gain, especially in midlife.
There’s a lot of info here, so to make it easier I’ve created a quick reference guide so you know the basics and action steps at a glance. I’ve even included a bonus reason we can gain weight in midlife.
Now tune into the Ounce of Prevention Chat below as we dive deeper into how Estrogen effects weight loss at Midlife.
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