我想起以前在睡眠中心跟診時發生的事情。醫生都很喜歡預判（大概？），我們那時候很希望能找到一種方式，知道這個BMI大於30（或在30那邊了）的人，需不需要乓尬ㄙ。這是為了要區分OSA(肥胖相關的阻塞性睡眠呼吸中止症)是不是合併有hypoventilation(低通氣換氣症候群)，黃金準則是清醒狀態抽動脈血，看有沒有二氧化碳堆積。但因為抽動脈血會連帶一些沒有人喜歡冒的風險，而且成本較高（各方面來說），所以也不是BMI超過30就要抓去抽動脈血這麼簡單可以解決的。
總之那天門診有個年輕人就是BMI 30(其實看起來不胖，頂多會說他結實)，然後所有血液檢驗都正常。主任說：「那魏醫師，你怎麼看？」（突然拋球？！
「痾，雖然體重算是過重，但基本上還算健康。」被主任和病人一起看著的我回答。
然後主任就回頭對病人說：「恭喜你，魏醫師說你是健康的胖子。」
( ( ⁰▱⁰ )！！！！）
我到現在還是覺得主任語帶諷刺。
其實我很怕自己變成那種，只會看數字是不是紅字，只看標準指引，就去做判斷和做處置的醫生。例如我還是覺得需不需要減重，或是需不需要特別去長期吃藥控制血脂等等問題，還是要依據當事者狀況去和本人討論和決定。
我身邊也有那種「我都年紀這麼大了還要跟你們一樣做什麼量體重？」「我自己知道自己身體要什麼」的長輩。又看他們這樣的飲食習慣，也過得蠻開心的，沒什麼慢性病，我也覺得刻意去「矯正」他們的意義在哪？我又有什麼權利去做這種事呢？
總之到底要不要干涉，又要干涉到什麼程度，一直很難拿捏啊。
不過，關於「健康型肥胖」還是「不健康型肥胖」，以及有的OSA有OHS有的人不會，差異在哪？目前都還是覺得處於生理到病理之間連續光譜的某個位置上，也可以看作是病理化的初期和後期，所以也不是不維持健康體重，或是不治療的藉口就是了。
𐂂𓈒𓐍𓂃𓈒𓂂
代謝健康型肥胖是指身體質量指數(BMI)在肥胖範圍(≥ 30 kg/m²)，但並沒有出現肥胖相關代謝併發症的人。也就是說，雖然他們的BMI很高，但血壓、血糖和血脂的數值都在健康範圍。
大約 10%–25% 的高 BMI 族群沒有出現代謝併發症，例如高血糖或內臟脂肪堆積。
那是不是代表這種健康型肥胖其實大有人在?
大約 10%–25% 的高 BMI 族群沒有出現代謝併發症，例如高血糖或內臟脂肪堆積。
那是不是代表這種健康型肥胖其實大有人在?
Metabolically healthy obesity (MHO) describes individuals who do not display metabolic complications typically associated with obesity, despite having a Body Mass Index (BMI) in the obese range (≥ 30 kg/m2). In other words, while they have a high BMI, these individuals have healthy blood pressure, blood sugar, and lipid levels.
Roughly 10%–25% of people with a high BMI do not show immediate metabolic complications, such as high blood sugar or fat around organs.
Does that mean there are quite a few healthy obese people?
Roughly 10%–25% of people with a high BMI do not show immediate metabolic complications, such as high blood sugar or fat around organs.
Does that mean there are quite a few healthy obese people?
代謝健康型肥胖並不是什麼新概念，還記得「梨形身材」和「蘋果身材」嗎? 現在我們也知道不同種族和地區的人，體脂肪分佈存在顯著的差異。這意味著兩個BMI相同的人，其內臟脂肪和皮下脂肪的含量可能大相徑庭。
南亞和東亞人種即使在BMI較低的情況下，內臟脂肪和腹部脂肪也較高。這導致他們即使體重不算多胖，罹患第二型糖尿病和胰島素阻抗的風險還是較高。
南亞和東亞人種即使在BMI較低的情況下，內臟脂肪和腹部脂肪也較高。這導致他們即使體重不算多胖，罹患第二型糖尿病和胰島素阻抗的風險還是較高。
Metabolically healthy obesity is not a new concept. Remember “pear-shaped body” v.s. “apple-shaped body”? Now we also know significant racial and regional differences exist in body fat distribution, meaning that two people with the same BMI can have vastly different levels of internal (visceral) and subcutaneous (under-the-skin) fat depots.
South & East Asians have higher visceral fat and abdominal adiposity even at low BMIs (“thin-fat” phenotype). This lead to a higher risk of Type 2 diabetes and insulin resistance at lower weights.
South & East Asians have higher visceral fat and abdominal adiposity even at low BMIs (“thin-fat” phenotype). This lead to a higher risk of Type 2 diabetes and insulin resistance at lower weights.
但即使都屬亞洲，不同族群的體脂分佈仍存在差異。南亞人（例如印度人）在相同的BMI，通常體脂率和內臟脂肪含量最高，其次是東南亞人（例如馬來人）和東亞人（例如中國人）。此外，印度和馬來西亞一些快速都市化的地區導致了「脂肪外溢」現象，即天生的體質與攝取加工食品的加乘作用之下，導致內臟脂肪的急劇增加。
「脂肪外溢」是指功能失調的脂肪組織無法再充分儲存飲食攝入的脂肪，導致過量的脂質溢出到血液中，並在器官和內臟中積聚成對健康有害的「異位脂肪」。
「脂肪外溢」是指功能失調的脂肪組織無法再充分儲存飲食攝入的脂肪，導致過量的脂質溢出到血液中，並在器官和內臟中積聚成對健康有害的「異位脂肪」。
But even within Asia, patterns vary. South Asians (e.g., Indian) typically have the highest body fat and visceral adiposity for a given BMI, followed by Southeast Asians (e.g., Malay) and East Asians (e.g., Chinese). Moreover, rapid urbanization in regions like India and Malaysia has led to “lipid spillover,” where traditional genetic traits interact with processed diets to drastically increase visceral fat deposits.
“Lipid spillover” is a pathological mechanism where dysfunctional adipose tissue can no longer adequately store dietary fats, causing excess lipids to overflow into the bloodstream and accumulate as toxic “ectopic fat” in organs and visceral depots.
“Lipid spillover” is a pathological mechanism where dysfunctional adipose tissue can no longer adequately store dietary fats, causing excess lipids to overflow into the bloodstream and accumulate as toxic “ectopic fat” in organs and visceral depots.
與相同BMI的非裔黑人和歐洲白人相比，西班牙裔/拉丁裔人種的軀幹（腹部）脂肪百分比以及整體脂肪含量都更高。這導致他們容易罹患代謝症候群和脂肪肝。
黑人/非裔人種的皮下脂肪含量較高，但內臟脂肪和肝臟脂肪含量顯著低於白人和亞洲人。因此，使用BMI可能會高估他們的疾病風險；然而，基於其他因素，他們罹患心血管疾病的風險仍然很高。
黑人/非裔人種的皮下脂肪含量較高，但內臟脂肪和肝臟脂肪含量顯著低於白人和亞洲人。因此，使用BMI可能會高估他們的疾病風險；然而，基於其他因素，他們罹患心血管疾病的風險仍然很高。
Hispanic/Latinos have higher trunk (abdominal) fat percentages and higher total body fat for a given BMI than Black and White counterparts. This leads to an increased susceptibility to metabolic syndrome and fatty liver.
Black/Africans have higher subcutaneous fat but significantly lower visceral and liver fat compared to Whites and Asians. So using standard BMI may overestimate their health risks; however, they remain at high risk for CVD due to other factors.
Black/Africans have higher subcutaneous fat but significantly lower visceral and liver fat compared to Whites and Asians. So using standard BMI may overestimate their health risks; however, they remain at high risk for CVD due to other factors.
白人/歐洲人的內臟脂肪在所有人種之中處於中等，而他們腿部的脂肪和全身脂肪含量往往高於非裔黑人。現行的標準BMI臨界值很大程度上是基於這一人種制定出來的。
大洋洲和亞洲部分地區的人種，遺傳上則表現出效率特別高的脂肪儲存傾向（「節儉基因」的傳承），這可能是來自這些地區自古以來得適應飢荒-豐饒反覆變化之週期，所以演化出這樣的體質。
因紐特人和波利尼西亞人與腰圍相同的白人相比，血壓更低、血脂數值更好，因為他們天生對皮下脂肪的耐受性更高。
大洋洲和亞洲部分地區的人種，遺傳上則表現出效率特別高的脂肪儲存傾向（「節儉基因」的傳承），這可能是來自這些地區自古以來得適應飢荒-豐饒反覆變化之週期，所以演化出這樣的體質。
因紐特人和波利尼西亞人與腰圍相同的白人相比，血壓更低、血脂數值更好，因為他們天生對皮下脂肪的耐受性更高。
White/Europeans have generally intermediate visceral fat levels; they often have higher leg and total fat mass than Black individuals. Standard BMI cut-offs were largely developed based on this population.
Some regions (like Oceania and parts of Asia) show a high genetic predisposition for efficient fat storage (“Thrifty Gene” legacy), likely an evolutionary adaptation to historical feast-and-famine cycles.
The Inuit & Polynesian group patterns often show lower blood pressure and better lipid profiles than White populations for the same waist circumference, suggesting a higher tolerance for subcutaneous fat.
Some regions (like Oceania and parts of Asia) show a high genetic predisposition for efficient fat storage (“Thrifty Gene” legacy), likely an evolutionary adaptation to historical feast-and-famine cycles.
The Inuit & Polynesian group patterns often show lower blood pressure and better lipid profiles than White populations for the same waist circumference, suggesting a higher tolerance for subcutaneous fat.
代謝健康型肥胖主要取決於脂肪在體內的儲存位置和方式，而不僅僅是脂肪總量。具體而言，臀部、髖部和大腿有保護性緩衝作用，其特性與腹部脂肪不同，它分泌較多的脂聯素和瘦素，產生的促發炎細胞因子（如IL-6）較少。此外，它脂肪分解的速度也較低，還能夠捕捉循環中過量的脂肪酸並長期儲存，預防異位脂肪堆積；當這些「儲存庫」健康的擴張時，可以防止「脂質外溢」到肝臟、心臟和骨骼肌等危險的異位部位，少了這道保護機制，就容易導致胰島素抗性和第二型糖尿病。反之，腹部脂肪組織則是會將脂肪直接釋放到門靜脈循環中。
Metabolically Healthy Obesity (MHO) is largely determined by where and how the body stores fat, rather than just the total amount. Specifically, the gluteofemoral depot has unique intrinsic properties that differ from abdominal fat. It secretes higher levels of adiponectin and leptin, while producing fewer pro-inflammatory cytokines like IL-6. And it has a lower rate of fatty acid release (lipolysis) and traps excess circulating fatty acids for long-term storage. When this “sink” expands healthily, it prevents “lipid spillover” into dangerous ectopic sites like the liver, heart, and skeletal muscle, which otherwise leads to insulin resistance and type 2 diabetes, while abdominal depots release fat directly into the portal circulation.
另一個差異在於脂肪組織擴張的方式。 「健康」的脂肪組織會透過「增生」，也就是產生新的、小的脂肪細胞。這有助於維持良好的血液循環（血管新生）和健康的荷爾蒙平衡。不健康的脂肪組織則是透過「肥大化」來擴張，這意味著現有的脂肪細胞會膨脹到巨大的體積。這些過度膨脹的細胞常常會發炎、缺氧，並外溢出脂肪酸，導致「不健康/病態型」的肥胖。
Another difference depends on “how” these adipose tissues expand. “Healthy” adipose tissue grows by hyperplasia, creating new, small fat cells (adipogenesis). This maintains good blood flow (angiogenesis) and a healthy hormonal profile. Unhealthy adipose tissue grows by hypertrophy, which means existing fat cells simply swell to a massive size. These overstuffed cells often become inflamed, hypoxic, and leak fatty acids, leading to the “unhealthy” obesity phenotype.
一般來說我們很難對自己的基因動手腳，不過基因並沒有決定一個人健康的一切，飲食和運動以及環境因素都會共同作用，能夠影響你遺傳的脂肪分佈體質和代謝傾向。
環境因素可造成表觀遺傳改變，這種改變不需要改變DNA序列即可開啟或關閉基因。飲食和運動可以改變肥胖相關基因（如FTO）的DNA甲基化，可能減弱其負面影響。此外，運動還能調節microRNA和IL-6等路徑，這些都有助於維持肌肉質量和控制全身性發炎。即使遺傳因素很強，運動也能顯著減少內臟脂肪並改善胰島素敏感性，有可能防止從代謝健康型肥胖 (MHO) 轉變為不健康的肥胖。
Generally, it's difficult to manipulate our genes. However, genes don't determine everything about a person's health. Diet, exercise, and environmental factors all work together to influence your inherited body fat distribution and metabolic tendencies.
Environmental factors can cause epigenetic changes, which turn genes on or off without changing the DNA sequence itself. Diet and exercise can alter DNA methylation in obesity-related genes like FTO, potentially “muting” their negative effects. And exercise also modulates micro-RNAs and pathways like IL-6, which help maintain muscle mass and control systemic inflammation. Even if genetic factors are strong, exercise can significantly reduce visceral fat and improve insulin sensitivity, potentially preventing the transition from Metabolically Healthy Obesity (MHO) to unhealthy obesity.
攝取含糖飲料或油炸食品會加劇遺傳體質導致的BMI升高。這種影響在攜帶FTO等高風險基因變異的族群中最為顯著。
基因組成也可能決定哪種特定飲食（例如低脂或低碳水化合物飲食）對個人來說最有效。例如，低脂飲食對IRS1 CC基因型個體比較有效，而攜帶PPM1K T等位基因的個體遵循低碳水化合物飲食能夠減重更多。
Consuming sugar-sweetened beverages or fried foods accentuates genetic predisposition to elevated BMI. This effect is most pronounced in those with high-risk variants of genes like FTO.
Your genetic makeup may determine which specific diet—such as low-fat or low-carbohydrate—is most effective for you. For example, the low-fat diet intervention was found to be more effective for individuals with the IRS1 CC genotype, while those carrying the PPM1K T allele may lose more weight on a low-carbohydrate diet.
☽︎︎.* 𓃹
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