我们的这部分Facts on Fats 评论更详细地解释了膳食脂肪在人体中的不同功能，涵盖了（国际）国家权威机构对脂肪的膳食建议，并通过查看整个欧洲当前的消费水平讨论了人们在多大程度上遵守这些建议.本综述的一个重要部分致力于营养科学在膳食脂肪消耗与健康结果（包括肥胖和心血管疾病）之间关系方面的最新进展。为了更容易理解当前文档，该文档是为更高级的读者编写的，可能值得先阅读脂肪的功能、分类和特征 .
1。为什么膳食脂肪很重要？
脂肪的功能、分类和特性 描述了脂肪在味觉感知中的作用以及脂肪在许多食品技术应用中的重要性。从营养的角度来看，膳食脂肪对于与健康相关的几个方面和人体的最佳功能都很重要。膳食脂肪不仅仅是能量的来源；它们充当身体的结构构件，携带脂溶性维生素，参与体内重要的生理过程，并且对于包括生长和发育在内的许多重要生物功能都是必不可少的。下面将更详细地解释膳食脂肪的重要性。
提供能源
脂肪是人类饮食中的一种能量来源，另外两种主要的常量营养素是碳水化合物和蛋白质。脂肪是最集中的来源，每消耗 1 克可提供 9 大卡热量，这是蛋白质或碳水化合物能量含量（每克 4 大卡）的两倍多，是纤维能量含量（每克 2 大卡）的四倍多。脂肪可以储存在身体的脂肪组织中，当需要能量时，脂肪组织会释放脂肪酸（见方框：身体脂肪）。
结构组件
我们体内细胞周围的膜在物理上将细胞的内部和外部分开，并控制物质进出细胞的运动。它们主要由磷脂、甘油三酯和胆固醇组成（参见脂肪的功能、分类和特性 ）。来自磷脂和甘油三酯的脂肪酸的长度和饱和度都会影响膜的排列，从而影响其流动性。较短的链脂肪酸和不饱和脂肪酸的硬度和粘性较低，使膜更柔韧。这会影响一系列重要的生物学功能，例如细胞将自身包裹在颗粒周围以允许其摄取的内吞过程。
大脑的脂肪非常丰富（60%），并具有独特的脂肪酸组成；二十二碳六烯酸 (DHA) 是主要的脑脂肪酸。视网膜的脂质中也含有非常高浓度的DHA。
维生素的载体
在饮食中，脂肪是脂溶性维生素 A、D、E 和 K 的载体，并支持它们在肠道中的吸收。因此，摄入足量含有这些维生素的脂肪食物对于摄入这些微量营养素至关重要。
其他生物学功能
我们的身体不能产生脂肪的功能、分类和特征中描述的多不饱和脂肪酸 (PUFA) 亚油酸 (LA) 和 α 亚麻酸 (ALA) .如果没有这些必需脂肪酸，一些重要的功能就会受到损害，因此它们必须由饮食提供。 LA 和 ALA 可以转化为长链脂肪酸和具有激素样或炎症特性的化合物（例如分别为前列腺素或白三烯）。因此，必需脂肪酸参与许多生理过程，例如凝血、伤口愈合和炎症。虽然身体能够将 LA 和 ALA 转化为长链形式的花生四烯酸 (AA)、二十碳五烯酸 (EPA)，以及在较小程度上转化为二十二碳六烯酸 (DHA)，但这种转化似乎有限。长链脂肪酸 EPA 和 DHA 被认为是“有条件必需的”，建议直接食用这些特定长链脂肪酸的来源。 EPA 和 DHA 最丰富的来源是油性鱼类，包括鳀鱼、鲑鱼、金枪鱼和鲭鱼。查看脂肪的功能、分类和特征 更完整地了解最常见的脂肪酸及其所在的食物。
| 所有动物细胞都含有胆固醇，这是一种在细胞膜的流动性和渗透性中起作用的脂质。胆固醇也是维生素 D、肾上腺和性类固醇激素以及乳化和增强肠道吸收脂肪的胆汁盐的前体。胆固醇的主要膳食来源是奶酪、鸡蛋、牛肉、猪肉、家禽和（壳）鱼。 膳食胆固醇有助于维持稳定的胆固醇池，但胆固醇也由肝脏合成。人体调节其胆固醇状态。当胆固醇摄入量非常低时（如不食用动物产品的素食主义者），肠道吸收和合成都会增加。当胆固醇摄入量高时，身体的合成受到抑制，通过胆汁盐的排泄增加。每天通过小肠的胆固醇量（即膳食胆固醇和产生的胆固醇的总和）在 1 到 2 克之间。欧洲的平均胆固醇摄入量为 200-300 毫克/天，这意味着身体的生成量明显更高。血液胆固醇水平是肠道吸收和肝脏合成的净结果，减去通过粪便排泄（如胆固醇、胆汁盐和细菌转化产生的产物）和细胞对胆固醇的使用。 重要的是，对于大多数人来说，食用含有胆固醇的食物对血液中的胆固醇水平影响不大（另见第 3 节中的建议）。然而，少数人（占人口的 15-25%）可能对膳食胆固醇“过度反应”，因此建议限制他们的胆固醇摄入量。 血液中的胆固醇由脂蛋白携带：LDL（低密度脂蛋白）和 HDL（高密度脂蛋白）。血液中这些脂蛋白的不同水平与健康的关系将在第 5 节中进一步解释。 |
2。膳食脂肪消耗量，有什么建议？
本节介绍了由世界卫生组织 (WHO) 和欧洲食品安全局 (EFSA) 等不同国际机构以及多个欧洲国家的国家政府和卫生当局发布的脂肪膳食建议。每隔几年就会对这些内容进行审查，并在查阅科学文献并咨询科学专家小组后，形成国家饮食建议和与健康相关的政策行动的基础。
从科学文献推断到实际的饮食建议可能因组织和/或国家而异。原因可能是这些建议是在较晚的时间发布的，在更新的研究结果可用之后，或者研究结果的解释略有不同。挑战之一是将研究结果转化为不同的健康相关结果，例如不同消费水平有益/有害的心脏病、癌症或死亡，纳入基于人群的建议。最重要的是，由于多种原因，研究结果并不总是很容易推断，包括选定的研究人群（例如 65 岁以上的糖尿病女性）、研究持续时间（较短的通常产生较弱的证据）或剂量和干预的组成（例如补充剂与全食物）。
因此，将不同研究的结果转化为针对一般人群的一般性建议是一项挑战。此外，没有标准的方法来定义饮食建议，背景文件并不总是清楚地说明所使用的程序。因此，在评估用于制定建议的科学证据时提高透明度是可取的。协调倡议正在解决这个问题，例如欧盟资助的 EURRECA 项目。
脂肪的饮食建议
从历史上看，饮食建议侧重于预防营养缺乏。这些指南旨在为人们提供健康饮食建议，以确保摄入足够的所有营养素。最近，随着肥胖和慢性病的患病率增加，营养建议已转向解决食物过度消费和预防慢性（代谢）疾病。
一般来说，体重管理的饮食建议包括控制总卡路里摄入量，并建议增加瘦肉、低脂乳制品、水果和蔬菜、全麦谷物和鱼类的摄入量。对于膳食脂肪，有人建议改变消耗的脂肪类型（即用不饱和脂肪代替饱和脂肪），或改变脂肪类型与整体减少脂肪相结合，可以预防心血管事件。
表 1 和表 2 概述了来自多个国家和国际权威机构和专业组织的成人对主要脂肪（表 1）和多不饱和脂肪酸（表 2）的建议。由于上述原因，这些建议因组织/国家而异。重要的是要记住，这些饮食参考值是针对人群而不是专门针对个人得出的。个人需求可能因许多个人和生活方式相关因素而异。
| %E 是指能量百分比，基于每日总能量建议，来自特定常量营养素（脂肪、碳水化合物或蛋白质）。对于正常体重的女性/男性，每日能量建议分别为 2,000/2,500 kcal，35%E 的建议来自总脂肪，相当于摄入约 78 g/97 g 脂肪。 |
表 1。 根据不同身体对成年人脂肪和脂肪酸摄入量的每日建议 - 改编自 Aranceta 等人。 2012
| 欧洲食品工业协会，2000 | 20-30%E | <10%E | <2%E* | |||
| 欧洲食品安全局，2010 | 20-30%E | 尽量低 | 尽量低 | |||
| 欧洲心脏病学会第四次联合工作组，2011-2012 | 25-35%E | <7%E | 加工食品尽可能低，<1%E来自天然来源 | |||
| 德国营养学会 (DGE)，2006 | 25-35%E | <10%E | <1%E | <300mg/天 | 7-10%E | |
| 英国营养委员会（COMA，1991） | 35%E | 10%E | 2%E | 12%E | 6%E | |
| 荷兰卫生委员会，2006-2011 | 20-40%E | <10%E | <1%E | <300mg/天 | (MUFA + PUFA:8-35%E) | 12%E |
| 安西斯，2011 年 | 35-40%E | ≤12%E | <2%E | 15-20%E | ||
| 桑特高等委员会。比利时，2009 | 30-35%E | <10%E | <1%E | <300 毫克/天 | >10%E | 5,3-10%E |
| 2012 年北欧营养建议 | 25-40%E | <10%E | 尽量低 | 10-20%E | 5-10%E | |
| 证监会。西班牙，2011 | ≤35%E | ≤10%E | <1%E | <350 毫克/天； <110 毫克/1000 大卡 | 20%E | 5%E |
| 美国农业部美国人膳食指南，2010 年 | 20-35%E | <10%E（用MUFA和PUFA代替） |
避免食用工业来源的反式脂肪 |
<300 毫克/天； | ||
| NHMRC。澳大利亚和新西兰，2013 年 | 20-35%E | SFA + TFA 合计不超过 10%E | ||||
| 粮农组织/世卫组织，2010 年 | 20-35%E | 10%E | <1%E* | 总脂肪 [%E]–SFA [%E]–PUFA [%E]–TFA [%E]； | 6-11%E |
表 2 .根据不同身体对成人多不饱和脂肪酸 (PUFA) 摄入量的每日建议 - 改编自 Aranceta 等人。 2012
总脂肪
大多数权威机构推荐成人膳食脂肪的总摄入量在 20-35%E 之间（见方框能量百分比）。这意味着建议每日总能量摄入的 20-35% 应来自脂肪的膳食来源。如第 2 节所述，脂肪具有许多重要的生物学功能，因此总消耗量不应低于 15-20%。此外，低脂肪饮食（≤20%E）可能会通过降低 HDL 和增加甘油三酯对血脂产生不利影响，并可能导致必需脂肪酸摄入不足。脂肪摄入量的上限旨在确保人们不会像脂肪一样消耗过多的每日卡路里，因为它是能量密度最高的常量营养素。
总脂肪摄入量的建议进一步细分为特定脂肪酸的建议摄入量。阅读脂肪的功能、分类和特性 有关脂肪酸分子结构和命名法的更多信息。
饱和脂肪酸
将饱和脂肪酸 (SFA) 消耗量保持在 10%E 以下的建议源于其 LDL 胆固醇升高的潜力和对心血管疾病 (CVD) 风险的影响。一些指南建议尽可能降低饱和脂肪的摄入量。人们普遍认为，当饱和脂肪酸被 PUFA 取代时，效果最为积极。
反式脂肪酸
反式脂肪酸 (TFA) 的建议主要是保持摄入量尽可能低或低于 1%E。令人信服地表明，TFA 会对血脂产生不利影响并增加随后的 CVD 风险。与 10 至 15 年前相比，最近在西欧分析的绝大多数食品中的反式脂肪酸含量都不含高水平的反式脂肪酸，也不会对健康构成重大风险。虽然在一些东欧国家发现 TFA 水平明显较高。
单不饱和脂肪酸
大多数饮食建议没有针对单不饱和脂肪酸 (MUFA) 的具体建议。粮食及农业组织 (FAO) 表示，可以通过以下计算获得 MUFA 建议：总脂肪 [%E] – SFA [%E] – PUFA [%E] – TFA [%E]，其中 15 -20结果是 %E。
多不饱和脂肪酸
并非所有（国际）国家当局都对总 PUFA 有具体建议，但有些有（表 1 和表 2）。相反，他们为特定脂肪酸设定了建议，包括 n-3 脂肪酸 ALA、EPA、DHA 和 EPA+DHA，以及 n-6 脂肪酸 LA，在某些情况下还包括 AA。这些建议在不同的国家、组织和消费者年龄组之间存在很大差异，并以“%E”或“g/day”表示（表 2）。造成这些差异的原因可能是因为一些组织专注于避免缺陷，而另一些组织则制定了预防慢性病的建议。
胆固醇
大多数权威机构没有提供胆固醇消耗的最大量。当他们这样做时，建议不要超过 300 毫克/天。最新的科学出版物指出，在健康个体中，饮食中的胆固醇对血液中的胆固醇水平几乎没有影响（见框胆固醇）。
3。我们消耗了多少膳食脂肪？
监测人群中膳食脂肪的消费水平，并评估人们对膳食指南的遵守程度对于评估建议的有效性很重要。
全球脂肪消耗
全球食品消费数据表明，总脂肪消耗水平平均在推荐的 20-35%E 范围内。然而，国家差异很大，从孟加拉国的 11.1%E 到欧洲显着更高的摄入量，希腊为 46.2%E。 2010 年，代表全球 61.8% 成年人口的数据表明，全球 SFA 平均摄入量低于建议的最大值 10%E (9.4%E)，其中东南亚棕榈油生产岛国的摄入量最高.在 PUFA 消费方面，1990 年至 2010 年间，全球 n-3 PUFA 的摄入量有所增加，但平均而言仍低于推荐值。同样，国家之间存在巨大差异；一项代表全球 52.4% 人口的研究发现，海产品和植物 n-3 脂肪酸的摄入量分别为 <50 至>700 毫克/天和 <100 至>3000 毫克/天。同样，n-6 PUFA (2.5-8.5%E) 的全球摄入水平低于推荐值。
欧洲脂肪消费
在欧洲，食物消费数据表明，总脂肪摄入量普遍高于推荐的 20-35%E（表 3 和表 4），最大摄入量从西方的 37%E 到西方的 46%E南方。查看特定脂肪酸，饱和脂肪消耗量显着超过所有地区推荐的最大值 10%E。中东地区的消费量最高，罗马尼亚的消费量超过 25%。然而，各国衡量消费的方法不同，这可能部分解释了观察到的差异。与 2004 年的上一份报告相比，目前总脂肪和饱和脂肪的摄入量略有下降。多不饱和脂肪酸 (5-8%E) 和单不饱和脂肪酸 (11-14%E) 的摄入量低于推荐值。有趣的是，在地中海国家，根据橄榄油的主要用途，MUFA 的摄入量是欧洲最高的。最近通过食品重新配制来减少膳食反式脂肪酸的行动导致整个欧洲的反式脂肪酸摄入量持续下降，低于低于 1%E 的建议值。
表 3. 四个欧洲地区成年人的能量和常量营养素摄入量（最小值-最大值）——改编自 Elmadfa 1 2009
| 9.2 - 11.1 | 13.7 - 16.8 | 42.4 - 51.0 |
18.0 - 25.0 | 31.0 - 44.9 |
| 6.8 - 8.2 | 13.7 - 17.2 | 42.9 - 51.0 |
15.6 - 21.0 | 31.0 - 41.9 |
| 9.1 - 10.4 | 14.1 - 18.5 |
36.8 - 47.0 |
19.3 - 23.5 | 28.4 - 45.0 |
| 7.1 - 8.7 | 14.4 - 19.3 |
37.7 - 50.1 |
16.9 - 23.7 | 29.9 - 47.2 |
| 9.0 -13.9 | 13.5 -17.8 | 42.5 - 49.5 |
18.7-29.7 | 31.3 - 38.9 |
| 7.5 -11.4 | 13.1 - 17.1 | 43.6 - 53.9 |
19.7 - 24.7 | 31.2 - 39.7 |
| 9.1 - 12.2 | 14.7 - 16.3 |
42.4 - 47.6 |
12.8 - 24.4 | 34.8 - 36.5 |
| 6.6 - 8.4 | 15.6 - 17.0 |
44.4 - 48.0 |
10.4 - 20.1 | 35.1 - 36.9 |
表 4. 欧洲四个地区成年人的脂肪、脂肪酸和胆固醇摄入量（最低-最高）——改编自 Elmadfa I 2009
| 地区/性别 | 脂肪 %E | SFA %E | MUFA %E | 多不饱和脂肪酸 %E | 胆固醇毫克 |
| 北 | |||||
| South | |||||
| Central / East | |||||
| West | |||||
4. How do dietary fats relate to our health?
This section explains in more detail the science underpinning the dietary recommendations. It provides an overview of the studies related to the consumption of dietary fat and its effect on a number of health related outcomes, but also describes findings from more recent work in the field of nutrition science that need further investigation. Only when a sufficient number of studies on humans consistently show a link between fat (or a specific fatty acid) and health, leading to a consensus between scientific experts, it may be incorporated in actual recommendations.
Although the major non-communicable diseases (NCDs) seem to be interrelated (e.g. CVD and cancer are often attributed to overweight and obesity, and type 2 diabetes affects blood lipids independently of body weight), the following overview of scientific studies is subdivided by disease/health condition.
Obesity
People who are affected by obesity or overweight have an increased risk for developing chronic diseases, such as CVD, metabolic syndrome, type 2 diabetes mellitus and certain types of cancer. Visceral fat that accumulates around the organs in the abdomen is particularly associated with higher risk of developing these diseases. Maintaining a normal body mass index (BMI) and waist circumference, as an indication of a healthy ratio between fat and lean body mass, is therefore important for staying healthy. WHO data from 2014 show that the prevalence of obesity [defined by a BMI over 30 (kg/m2)] worldwide has nearly doubled since 1980, and point to energy imbalance as the fundamental cause. Both physical inactivity and the increased intake of energy-dense foods are explicitly mentioned as an explanation for the global increase of obesity. Since having too much body fat seems harmful, it is reasonable to think that an increased dietary fat consumption is associated with higher body fat levels and a subsequent increased disease risk. But what is the scientific evidence behind this?
When more calories are consumed than used, an imbalance of energy occurs. With time, a sustained imbalance results in an increase of body weight and body fat. While fat contains the most calories per gram, compared to carbohydrates and proteins, there is no scientific evidence that shows an independent role of dietary fat in the development of overweight and obesity. Also, a low-fat diet without total calorie reduction will not lead to weight loss. In other words, a person is unlikely to gain weight on a high fat diet, if the total amount of recommended daily calories is not exceeded and energy expenditure is normal. Furthermore, fat and calorie restriction alone are not sufficient for long-term weight reduction, increased physical activity is also required.
| There are two types of body fat (or adipose tissue):white (WAT) and brown adipose tissue (BAT). Adipose tissue In humans, fat tissue is located under the skin (subcutaneous fat), around the organs (visceral fat), in bone marrow (yellow bone marrow) and in breast tissue. These fat deposits are used to meet energy demands when the body needs it, for normal daily activities, but also when energy requirements are higher such as during high levels of physical activity, pregnancy, lactation, infancy and child growth and in the case of starvation. Although its main function is energy storage, fat tissue is more metabolically active than previously thought. It contains many small blood vessels and fat cells – adipocytes. Adipocytes produce and secrete a broad array of proteins and other molecules such as leptin, adiponectin, tumor necrosis factor-α (TNF-α), and interleukins 6 and 1β (IL-6, IL-1β) that are important for immune responses in host defence and play roles in reproduction (estradiol) and energy/lipid metabolism. Fat deposits also help to insulate the body and cushion and protect vital organs. But, excess body fat, especially visceral fat is associated with insulin resistance, impaired fatty acid metabolism and increased cardiovascular risk. A high accumulation of visceral fat around the organs may lead to the typical ‘apple shape’ figure. However, it is important to recognise that a person can appear lean and still have a relatively high percentage of body fat. Brown fat Whereas WAT is mainly used for energy storage, BAT contains more mitochondria (energy producing cell components) and has the capacity to generate heat by burning triglycerides. Hybernating animals are known to use BAT to keep the adequate body temperature while in resting state. In humans, this specific type of tissue has previously only been known in babies. There are now indications that similar heat-producing cells are also present in human adults, which may be activated through a reduction in body temperature. Surrounding temperature therefore influences the energy balance by increasing the energy expenditure. Potential long-term implications for weight management have yet to be investigated. |
Blood lipid profile &cardiovascular disease
According to the WHO, CVD is the number one cause of death globally, accounting for 30% of total mortality. In the 1970s, a link between total/saturated fat consumption and the risk for heart disease mortality was established in the Seven Countries’ study, which led to nutrition recommendations by several authoritative bodies to reduce saturated and total fat from the diet, to prevent CVD. However, more recent studies in nutrition science point out that an independent relation between fat intake, especially saturated fat, and cardiovascular conditions, has not been consistently shown. In fact, it has become more evident that a replacement of SFA by PUFA reduces the risk for CVD.
Research in this area consists mainly of 1) intervention studies in which the effect of a certain diet, e.g. high in saturated fat, on blood lipid levels is examined, and 2) observational studies that investigated the association (not cause-effect relation) between the consumption of dietary fat and the incidence cardiovascular events, e.g. heart attacks or strokes, over a long period of time. An overview of the available scientific studies is described below.
Blood lipid profile
Intervention studies on the effects of fat intake on CVD have mainly studied the effects of a reduction in total/saturated dietary fat (replaced by other nutrients) on the levels of blood lipids. Abnormal blood lipid levels are a risk factor for developing CVD. A higher risk is indicated mainly by high levels of LDL (“bad”) cholesterol, but also an increased ratio between LDL (or total) cholesterol and HDL (“good”) cholesterol. This ratio is suggested to be a better marker for CVD risk than LDL alone. In addition, recent research indicates that Apo A1 and Apo B (proteins that are involved in lipid transport in the body) blood levels, and the size of the LDL particle, may be good risk markers for CVD. A smaller LDL particle size is more likely to induce atherosclerosis - the formation of plaques on the inside of blood vessels that increases the risk of blockage and subsequent (cardio) vascular events. An elevated level of blood triglycerides is also linked to a higher risk of CVD.
There is evidence that lowering saturated fat intake has a positive effect on LDL cholesterol and the total/HDL cholesterol ratio, and subsequently on the CVD risk, but only if SFA are replaced by PUFA (both the n-3 and n-6), and not by digestible carbohydrates such as starch or glucose. In some intervention studies, replacement of saturated fat by digestible carbohydrates has been linked to a more atherogenic blood profile and dyslipidaemia (elevated triglyceride levels, decreased HDL cholesterol and smaller sized LDL particles). Also, replacement of SFA by MUFA shows positive effects on blood pressure and blood lipid profile; but these effects are not as strong as those of PUFA. Intervention studies also show that replacing digestible carbohydrates with MUFA has positive effects on raising HDL cholesterol, lowering LDL cholesterol and the total/HDL cholesterol ratio, and may improve insulin sensitivity.
The effects of SFA on the blood lipid profile may be further broken down into the effect of individual SFA, as it may vary for fatty acids with different chain lengths. However, there is currently insufficient evidence to link any specific saturated fatty acid to a strong adverse effect on blood lipids or a disease endpoint. SFA with a shorter carbon chain (e.g. lauric acid) do increase LDL cholesterol stronger than the ones with a longer chain, e.g. stearic acid, but at the same time the former also have a higher HDL-raising potential. The short-chain fatty acids may show more positive effects on the total/HDL cholesterol ratio. A recent review shows that palmitic acid, the most abundant saturated fatty acid in the diet, seemed to increase LDL cholesterol, but also HDL cholesterol, and has not been shown to increase the risk for CVD. With data on the relation between specific SFA and CVD endpoints lacking, the total body of evidence is insufficient to favour one SFA over another regarding CVD benefits and further research is needed to confirm any differences in health effects between these fatty acids.
The adverse health effects of TFA, have been consistently shown, not only in comparison with PUFA, but also compared to saturated fat, and the effects are not limited to blood lipid levels and CVD. TFA also induce low-grade inflammation and may, particularly in individuals predisposed to insulin resistance, decrease insulin sensitivity which is related to the development of type 2 diabetes. Limited data show that both industrial and ruminant TFA seem to exert similar effects when consumed in the same amounts, but very rarely people consume high enough amounts of ruminant TFA to be comparable to that from industrial sources.
Cardiovascular disease
Meta-analyses of observational studies, which look at the long-term effects of consumption on the actual disease outcome, indicate that:1) there is no independent association between the consumption of saturated fat and the risk for CVD, and 2) replacement of saturated fat by PUFA, rather than digestible carbohydrate or MUFA, lowers the risk for CHD. A Cochrane review found a reduction of CVD risk in studies of fat modification (i.e. SFA replaced by MUFA/PUFA) when studies lasted at least two years; the reduction was found in men, but not in women. Replacing 5% of energy intake of saturated fat by PUFA, would result in a 10% CVD risk reduction. Similarly, it was estimated that, in populations consuming a Western-type diet (a diet high in refined grains, fat and sugar, and low in wholegrain), the replacement of 1% of energy from saturated fat with PUFA lowers LDL cholesterol, and is likely to produce a reduction in CHD incidence of 2 to 3%. The European Food Safety Authority (EFSA) Panel on Dietetic Products, Nutrition and Allergies (NDA) has concluded that a cause and effect relationship has been established between the consumption of mixtures of dietary SFA and an increase in blood LDL-cholesterol concentrations, and that replacement of a mixture of SFA with cis-MUFA and/or cis-PUFA in foods or diets on a gram per gram basis reduces LDL cholesterol concentrations. This scientific opinion relates specifically to low fat spreadable fats (margarine). It has been suggested that this may be partly related to the anti-inflammatory properties of n-3 fatty acids. Furthermore, a relationship was found between n-3 fatty acids and a lower total mortality risk, largely attributable to fewer cardiovascular deaths. Individuals with the highest n-3 fatty acid levels lived on average 2.22 years longer, after the age of 65 years.Two recent large studies investigated the effects of n-6 fatty acids on the risks of death and coronary heart disease, respectively. They concluded that linoleic acid, the main n-6 fatty acid, lowered the risk for both these endpoints.
There is currently no scientific evidence for a link between individual SFA (e.g. lauric acid, stearic acid or palmitic acid) and CVD risk. For TFA on the other hand, there is scientific consensus about the link between consumption and an increased risk of developing CVD.TFA consumption from ruminant sources, such as dairy and meat, has not been related to disease endpoints, probably because the intake levels from ruminant derived products were significantly lower than from industrial sources when these studies were performed. However, evidence is insufficient to establish whether there is a difference between ruminant and industrial TFA consumed in equivalent amounts on the risk of coronary heart disease.
Type 2 diabetes
The effect of fat consumption per se on the development of type 2 diabetes is not clear, since much of the risk seems to be related to overweight. However, there are some indications that the type of dietary fat can influence where fat accumulates in the body, with SFA leading to more fat around the organs, including liver, which is linked to type 2 diabetes.
Changing the types of fat (PUFA instead of SFA), rather than reducing the total amount of fat in the diet, may also have a positive effect on glucose metabolism.Animal studies have shown improvement of several metabolic factors, including insulin sensitivity, underlying the development of type 2 diabetes when SFA are replaced with PUFA. Insulin sensitivity refers to the capacity of body cells to respond to the hormone insulin, which supports the uptake of glucose, amino acids and fatty acids. A 12-week n-3 PUFA supplementation in people with obesity, insulin resistant children and adolescents, showed positive effects on blood lipids and insulin sensitivity. However, two recent meta-analyses did not find evidence for fish and n-3 fatty acid consumption to lower the risk for type 2 diabetes in humans.
There seems to be a relation between insulin resistance and the way the body responds to fat intake. People with insulin resistance respond less favourably to a diet lower in total and saturated fat (aiming to lower CVD risk) than people who respond normally to insulin. Moreover, being insulin resistant is associated with an increased risk for CVD, even at moderate LDL-cholesterol concentrations in the blood.
Inflammation
Chronic low-grade inflammation in fat tissue of individuals affected by obesity has been associated with the pathogenesis of insulin resistance and the development of the so-called metabolic syndrome. What actually causes the inflammation is unknown, but several factors may be involved, including the activation of innate immune processes by SFA. The n-3 fatty acids, EPA and DHA, on the other hand, may have anti-inflammatory properties that modulate adipose tissue inflammation.
A low n-6/n-3 or LA/ALA intake ratio has been proposed to have an anti-inflammatory effect, and therefore to be beneficial for cardiovascular health. However, there is no consensus about this marker, based on the current available evidence and conceptual limitations of the use of this ratio. Losing weight and thereby reducing adiposity seems an efficient strategy to lower inflammation, and improve fatty acid metabolism and insulin sensitivity.
Cancer
Similar to the risk of diabetes, excessive body weight increases the risk of developing different types of cancer, which may explain why in some countries the prevalence for this disease is higher. The current scientific evidence is limited and does not confirm a strong association between total and specific fatty acids intake and development of cancer. The joint initiative of World Cancer Research Fund and American Institute for Cancer Research reported that there is little evidence to suggest a link between total fat intake and breast, lung or colorectal cancers. Whereas emerging evidence suggests that a higher level of n-3 fatty acid consumption may be associated with reduced risk of certain cancers, for n-6, this does not seem to be the case.
Neurological health, cognitive functioning &dementia .
The n-3 fatty acid DHA is an import
