#Normalweight

[dykemd]

some people get tipsy on half a beer so consider urself normalweight 👍

ure right i should be grateful i get to enjoy up to 3 beers sometimes n i wish u could feel what i feel 🫂

[venovenous]

If anyone wants to ask if I got fat the answer is no: i am simply no longer underweight and severely mentally ill. now I am normalweight for a male my size and mild to moderately mentally ill

[zoya-thinks]

Come here and Calculate your Body Mass Index. Take a moment to know about your Weight Status.

[lifestyle-transformation-blog]

Classification of body weight based on BMI a.k.a Body Mass Index #life_styletransformations #bmi #obese #obesity #underweight #normalweight #overweight #fit #fitness #coach https://www.instagram.com/p/Ce3yodphZ8O/?igshid=NGJjMDIxMWI=

[recovery-anorexia]

The weight I always wanted to have! objective reached! goal reached!

[femsolid]

A few years ago, I gave a presentation on self-objectification to a room full of psychologists. I was discussing how self-objectification leads to high levels of body shame in women and what we might do to reduce it. A colleague interrupted me with a question. “Wait,” he said, “isn’t it maybe good that women feel shame about their bodies? Maybe you should feel bad if you gain weight. It could keep you from gaining weight.” I’ve heard some variant of that question many times since that day, though rarely so politely. Recently I received a slew of angry emails in response to a New York Times op-ed I wrote. My basic arguments were that fat talk and body shaming aren’t good for women, and that we’re wrong when we assume that body shaming motivates healthy behaviors. The authors of these rant-filled emails (all men) took me to task for suggesting that body shame was a bad idea. They proposed that shame is a necessary antidote to the obesity epidemic. One went so far as to tell me that french women are all slim (not true, by the way) because french culture so effectively shames fat women. Another suggested that the very future of our country depended on women continuing to feel shame about their bodies. By suggesting that women shouldn’t have to feel bad about themselves all the time, I was literally putting our country at risk!

Let’s start by taking apart the idea that body shame provides a pathway to the ultrathin body ideal for women. Of all the research conducted on obesity, there is not one drop of evidence that fat shaming helps to move people toward thinness. In fact, the opposite is true. A research study in the Journal of Health Psychology showed that the more young women receive negative comments about their weight, the less likely they are to exercise. In a different study of over five thousand adults across the United States, results demonstrated that experiencing weight stigmatization and discrimination is associated with an increased likelihood of overeating and more frequent consumption of convenience foods.

When we’re in emotional distress, we will usually take action to try to make ourselves feel better, even if that means trading a short-term mood boost for less appealing long-term consequences. Feeling better may come in the form of a pint of ice cream or a bag of chips that relieves your emotional distress temporarily, but triggers a spiral of shame. You felt bad about your body, so you ate something to feel better, and now you feel even worse about your body. This is one of the routes through which experiencing weight stigmatization can lead directly to binge eating.

You absolutely do not need to have visible ribs, a thigh gap, or a perfectly flat stomach in order to be healthy. You’re kidding yourself if you think you can always tell by looking whether someone is healthy. In a study of over 5,000 adults led by the Albert Einstein College of Medicine, researchers came to a stark conclusion: in the United States there are many “normalweight” people (around 24 percent) who show poor cardiovascular and metabolic health, and there are many obese individuals (around 32 percent) who are metabolically healthy. Thanks in part to the pervasive nature of our beauty-sick culture, much of the purported emphasis on “health” is often a thinly veiled concern about aesthetics. The research above makes it clear that you can’t tell whether someone is healthy just based on their body weight, but even if you could, quite frankly, that’s no excuse to treat anyone badly. “Health” should never be a prerequisite for being loved or being treated with dignity and respect. Women who don’t meet our culture’s rigid beauty ideals don’t owe the world some demonstration of their metabolic rate or cardiovascular fitness in order to be treated well or to prove that they’re “just as good as thin women.”

You can see why I felt so incredulous when I received emails from strangers arguing that we need more fat shaming in this culture. Both weight-based discrimination and obesity have continued to increase over time—there’s no sign that one stops the other. I’m deeply skeptical of those who claim they’re trying to “help” women by shaming them for their body size or shape, or those who say they fat-shame because they are worried about women’s health. Don’t imagine for a moment that any woman in this culture who struggles with weight is under any illusions about what her body looks like compared to the ideal. There is never a need to point out this gap. You are not doing her a favor. She already knows, trust me. Given the rampant fat shaming in this country, how could anyone imagine that obesity is a result of the fact that we simply don’t make people who are fat feel bad enough about themselves? Please. Cruelty is not a health intervention. It’s nothing more than a misguided, self-righteous attempt to boost one’s own self-esteem.

Here’s what I have to say to everyone who seems to believe that we should encourage women to feel body shame in order to promote weight loss. Even if you’re not convinced by all the empirical data reviewed above, why would you ever want to employ a health intervention focused not on caring for one’s body and treating it well, but rather based on loathing your body? Why would you want women to hate such an intimate and important part of themselves? What we need instead is to feel so at home and comfortable in our bodies that taking care of them feels natural and automatic. You don’t take care of things you hate.

- Beauty Sick, Renee Engeln

[crimsonkingart]

Fun fuct: some weeks ago a person thought I'm almost normalweight. ((In italian normalweithg is normopeso, but isn't totally corretc, because in italian means healty weitgh, not normal.)) In any case I'm still very far from normalweight, and I want to say it, because it's important understand that you can lose weight slowly. Lose weight isn't a race, so take time and if you have panick attack, anxiety and similar, please, speak with a psychologist or a doctor who specializes in eating disorders. And if you don't feel comfortable with a healthcare professional, you can look for another one, because you can find the right person.

[slimlastforskolins]

Rollercoaster weight changes can repeat with second pregnancy, especially among normal-weight women -- ScienceDaily

Rollercoaster weight changes can repeat with second pregnancy, especially among normal-weight women — ScienceDaily

Everyone knows that gaining excess weight during one pregnancy is bad, but clinicians rarely consider weight gains and losses from one pregnancy to the next — especially in normal-weight women.

But researchers from Marquette University and the University of Michigan found that among normal-weight women, fluctuating weight gain and loss in the first pregnancy is often repeated in subsequent…

[maximusen]

#tbt #shorthaircut #beforelockdown #normalweight #whocares?

[biomedgrid]

Biomed Grid | Association Between Timp-3/Angiotensin II, Profile and Cardiac Remodeling in Patients with Essential Hypertension and Heart Failure with Mid- Range Ejection Fraction

Abstract

Background and Aims: Arterial hypertension (AH) is a leading cause for heart failure with mid-range ejection fraction (HfmrEF). The aim of our study was to:

1. Measure levels of tissue inhibitor of matrix metalloprotease-3 (TIMP-3) and Angiotensin II (AII) in sera of patients with AH and HFmrEF.

2. In sera of controls.

Material and Methods: 56 patients with AH and HfmrEF were examined, mean age 65.62±9.69; and 22 age and sex matched healthy subjects, mean age 56.4±5.53. 41 of patients were with hypertension mediated organ damage and 15 were without. Patients were divided in two subgroupssubjects with left ventricular hypertrophy (n=32); (HFmrEF+LVH) and subjects without left ventricular hypertrophy (n=24); (HFmrEF-LVH). ELISA was used for measuring AII and TIMP-3.

Results: Patients with HFmrEF-LVH showed higher levels of TIMP-3: 7.747 (1.21916.725) than HFmrEF+LVH 4.693 (2.06210.463); (KW=0.48; p=0.48) and healthy controls 6.460 (1.00712.520); (p>0.05), but not significantly. TIMP3 showed correlation with grade of AH (r=0.85; p=0.02) and stage of AH (r=-0.52; p=0.05); and PLVW (r=-0.40; p=0.03). Patients with HFmrEF+LVH showed statistically significantly higher levels of AII: 8.533 (1.47713.009) than HFmrEF-LVH 1.333 (0.4776.932) and healthy controls 1.539 (0.2745.218); (KW=3.48; p=0.04). AII correlated with TIMP-3 (r=-0.50; p=0.0001), hypertensive cerebrovascular damage (r=0.57; p=0.0009), DBP (r=0.30; p=0.05), stage with AH (r=0.47; p=0.001); CK-MB (r=0.42; p=0.002) and UA (r=0.35; p=0.02).

Conclusion: Our data suggest an association between changes in levels of TIMP-3/Angiotensin II profile and cardiac remodeling. Determination of serum TIMP-3/Angiotensin II profile may be a useful method for monitoring of development and progression of LVH.

Abbreviations: BMI- Body Mass Index; DBP- Diastolic Blood Pressure; HDL- High Density; Lipoprotein Cholesterol; HFmrEF+LVH- Mid-Range Ejection Fraction and Left Ventricular Hypertrophy; HFmrEF-LVH- Mid-Range Ejection Fraction Without Left Ventricular Hypertrophy; LDL- Low Density Lipoprotein Cholesterol; SBP- Systolic Blood Pressure

Introduction

Traditionally cardiac extracellular matrix (ECM) is thought to be a relatively inactive structure, which takes the role as scaffolding for cardiac myocytes and vessels. Recent studies show evidence that cardiac ECM is metabolically active and dynamic structure. Changes in cardiac ECM turnover are suspected of contributing to the genesis and progression of heart failure [1]. Degradation of ECM’s structural proteins occurs through the action of matrix metalloproteinases (MMPs), which are regulated by tissue inhibitor of metalloproteinases (TIMPs). TIMP-3 is the only TIMP that is ECM-bound and could exert tissue-specific effects [2,3]. However, the exact role of TIMP3 in hypertension remains to be understood. The detection of subclinical left ventricular hypertrophy (LVH) is made difficult by several factors. “Firstly, the clinical disease processes do not cause signs and symptoms; consequently, LV remodeling may remain an unrecognized and insidious process for a prolonged period of time. Secondly, LVH is not easily detectable using standard clinical means such as a patient’s history, physical exam or electrocardiography (ECG). Specialized testing tools are usually needed for that subspecialty expertise to perform and interpret” [4].

There is growing evidence that supports the notion that angiotensin II (AII) may directly cause cardiovascular and renal diseases, independent of its hypertensive effect. Thus, recent in vivo work, coupled with in vitro findings, has provided new insights into the molecular and cellular mechanisms of AII-mediated cardiovascular and renal diseases [5]. Angiotensin II exerts direct effects on vascular remodeling and function [6]. TIMP-3 could be implicated in the progression of vascular diseases, independently from its ability to inhibit MMPs. In this regard, in vitro and in vivo adenoviral overexpression of TIMP-3, but not TIMP-1 or -2, has shown to promote apoptosis in vascular smooth muscle cells. In vivo experiments have shown that this effect was not achieved when synthetic MMP inhibitor was used [7,8]. Arterial hypertension (AH) is a leading cause for large number of heart failure (HF) cases. Heart failure with mid-range ejection fraction (HFmrEF) is a syndrome, defined by: (1)-Left ventricular ejection fraction (LVEF%)-40-49%; (2)-Symptoms and/or signs of heart failure; (3a)-Elevated levels of natriuretic peptides; (3b)-At least one additional criterion: relevant structural heart disease (left ventricular hypertrophy/left atrial enlargement) or diastolic dysfunction- 2016 European Society of Cardiology (ESC) Guidelines for the diagnosis and treatment of acute and chronic heart failure [9].

MethodsClinical draft

All patients were residing in the vicinity of the Pleven University Hospital. Subjects’ sera were taken from October 2016 to May 2017. All the procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional or regional) and with the Helsinki Declaration of 1975, as revised in 2000. Approval of local Ethics Committee was obtained and informed consent from adult research participants was obtained too. The study group consisted of 56 patients with AH and HFmrEF, mean age 65.62±9.69. Forty-one of patients were with hypertension mediated organ damage (HMOD) and 15 were without. Patients were divided in two subgroups- subjects with mid-range ejection fraction and left ventricular hypertrophy (n=32), mean age 62.5±12.58 years (HFmrEF+LVH); subjects with mid-range ejection fraction without left ventricular hypertrophy (n=24), mean age 60.4±8.4 years (HFmrEF-LVH) (Table 1). These values were compared to serum TIMP-3/Angiotensin II profile in 22 age and sex matched controls with no family history of diabetes, atherosclerosis or hypertension, mean age 56.4±5.53 years.

Table 1: Clinical data of patients with heart failure with mid-range ejection fraction and left ventricular hypertrophy and without left ventricular hypertrophy and healthy controls.

Note 1: Data are presented as mean±SD

Hypertension-Mediated Organ Damage Assessment: All patients were examined for HMOD via anamnesis (for established cardiovascular or premature CVD, renal, cerebrovascular or ophthalmological damage) and physical examination and pulse pressure assessment (in older people) >_60mmHg.

Instrumental tests

a. Arterial blood pressure was measured using a standard anearoid sphygmomanometer, to the nearest 2 mmHg, in the dominant arm after at least 10-min rest in supine position.

b. ECG was performed for LVH assessment (Sokolow–Lyon index >35 mm, or R in aVL >_11 mm; Cornell voltage duration product >2440mm.ms, or Cornell voltage >28mm in men or >20mm in women).

c. Echocardiography was performed with General Electric (Vivid S5) with 4-MHz transducer. All measurements were obtained according to ESC 2015 criteria for Cardiac Chamber Quantification by Echocardiography [10]. Echocardiographic LVH [LV mass index: men >50 g/m2.7; women >47 g/m2.7 (height in m2.7); indexation for BSA may be used in normalweight patients; LV mass/BSA g/m2 >115 (men) and >95 (women)].

Laboratory tests

1. Serum uric acid, glucose were determined. Total cholesterol, triglyceride concentrations, HDL were measured by enzyme assay (Boehringer Mannheim, Mannheim, Germany). LDL was calculated via Friedewald formula.

2. Serum creatinine levels were measured and moderate CKD with eGFR >30–59 mL/min/1.73 m2 (BSA) or severe CKD eGFR <30 mL/min/1.73 m2 were assessed

If any HMOD was found, then patient was further consulted with a referring specialist (cardiologist, nephrologist, neurologist, ophthalmologist).

Elisa

Enzyme-linked immunosorbent assay (ELISA) was used for measuring AII and TIMP-3 levels. TIMP-3 levels were measured in serum samples using enzyme-linked immunosorbent assay (R&D Systems, Minneapolis, MN, DY973) according to the manufacturer’s instructions. Angiotensin II levels were measured in serum samples using enzyme-linked immunosorbent assay ALPCO Diagnostics (Salem, MA, USA, 74-ANGHU-E01) according to the manufacturer’s instructions.

Statistical analyses

The research data was processed with the computer programs EXCEL (Microsoft Corporation, Redmond, WA) and STATGRAPHICS plus (Manugistics, Rockville, MD) for WINDOWS. All results were described in tables, graphs, numerical values (mean ± SD, share indicators and correlations). For assessment and conclusions in the case of normal distribution the Student t-test, Fisher’s F-test (ANOVA) and post-hoc tests (LSD, Tukey HSD, Scheffe, Bonferroni, Newman-Keuls, and Duncan) were used, and for distribution, different from the normal – the K-W (Kruskal-Wallis)-test. The level of significance was determined as p < 0.05. In cases with different from normal distribution, median was used (M), together with first and third quartile Q1 and Q3; (twenty-fifth and seventy-fifth percentile P25 and 75P).

Results

Serum TIMP-3 levels in patients were lower than controls 5.051 (2.06210.463) vs. 6.460 (1.00712.520) (p>0.05), but not significantly. Patients with HFmrEF-LVH showed higher levels of TIMP-3: 7.747 (1.21916.725) in comparison with HFmrEF+LVH- 4.693 (2.06210.463); (KW=0.48; p=0.48) and healthy controls 6.460 (1.00712.520) (p>0.05), but not significantly. TIMP3 showed correlation with grade of AH (r=0.85; p=0.02) and stage with AH (r=-0.52; p=0.05); and PLVW (r=-0.40; p=0.03). AII levels in patients were statistically significantly higher than controls- 8.952 (1.86915.782) vs. 1.539 (0.274 5.218); (KW=2.77; p=0.05). Patients with HFmrEF+LVH showed statistically significantly higher levels of AII- 8.533 (1.47713.009) than HFmrEF-LVH 1.333 (0.4776.932) and healthy controls 1.539 (0.274 5.218); (KW=3.48; p=0.04). AII showed correlation with TIMP-3 (r=- 0.50; p=0.0001), hypertensive cerebrovascular damage (r=0.57; p=0.0009), DBP (r=0.30; p=0.05), stage with AH (r=0.47; p=0.001); CK-MB (r=0.42; p=0.002) and UA (r=0.35; p=0.02).

Discussion

The conceptual role for AII, as a local mediator of fibrosis, is suggested by studies in which circulating AII is chronically increased from either endogenous or exogenous sources [11]. Mounting evidence points towards an authentic signalling capacity for TIMPs distinct from their MMP-inhibitory activity. It also seems to play an important role in the regulation of apoptosis, cell survival, growth, migration, differentiation, angiogenesis, inflammation and overall ECM remodelling. Due to these mechanisms TIMPs could play a vital role in the process of cardiac remodelling [12,13]. A suggestion about a link between TIMPs and the renin–angiotensin-system is firstly given by Kang [14]. They identified human angiotensin- II-type-2-receptor as a novel TIMP-3 interacting partner, linking TIMP-3 with the renin–angiotensin system. Although, the pathophysiological roles and signaling mechanisms of angiotensin-IItype- 2-receptor are still largely unknown, but they were shown to be increased during hypertrophy and ischemic heart disease. Our results show decreased TIMP-3 levels and increased AII in all patients. Interestingly, the TIMP-3/AII profile is different according to presence of LVH. This can be described by the next findings: TIMP-3 levels in patients with HFmrEF-LVH are statistically significantly higher than those in HFmrEF+LVH. On the contrary- AII levels in HFmrEF-LVH are statistically significantly lower than these in HFmrEF+LVH.

These results can be summarized with the next two ratios:

i. Profile of patients with HFmrEF-LVH- increased TIMP-3/ decreased AII

ii. Profile of patients with HFmrEF+LVH- decreased TIMP-3/ increased AII

Our results are consistent with authors [15] who found that recovery of TIMP-3 content in the failing myocardium is associated with reversing cardiac remodeling, highlighting the influence of this critical matrix constituent in maintaining normal cardiac structure and function. We report the existence of an association between changes in levels of TIMP-3/Angiotensin II profile and cardiac remodeling. Determination of serum TIMP-3/Angiotensin II profile may be a useful method for monitoring of development and progression of LVH in patients with essential hypertension and heart failure with mid-range ejection fraction. This is a pilot study. Although these findings should be confirmed in a larger study, our data suggest that changes in the TIMP-3/AII balance may play an important role in the structural, functional, and clinical manifestations of cardiac remodeling. However further examination and prospective studies are needed to clarify the MMP-independent biological functions of TIMP-3 and fully understand its effects and exact relevance on contributing to the cardiac remodeling.

Conflict of Interest

Authors declare no conflict of interest

Read More About this Article: https://biomedgrid.com/fulltext/volume4/association-between-timp-3angiotensin-ii-profile.000753.php

For more about: Journals on Biomedical Science :Biomed Grid | Current Issue

[strinkstuff]

There's no reason to be biased against people who are overweight. They're people too, and they're just as capable of doing what normalweight and underweight people can do.

Videogames: you can choose from twenty different eyelashes!!!! oh but you can’t be fat

[thoughtfuldonuttale]

Who is Donut?

The boring introduction.

Recently I was searching for a weightloss  buddy but didn’t find one that had the same goals as me or was the same age-ish that me. It bummed me a lot so I thought that why not start my own help page for you guys? 

I’m someone you can ask question regarding weightloss. Been there done that. You can also just update me where you are on your journey and I’ll give feedback and post it if wanted so that you’ll have an opportunity to find your own buddy. If you are at a stage where you don’t know how to start I’ll help you. It’s totally free. I’ll give you a diet and workouts to fit your goal. Tips included.

I've been overweight since 2nd grade and it was really hard mentally. I hit rock bottom when I was 13. I wanted to kill myself. Very dramatic, I know. I had been bullied about my weight for many years. I knew nothing about weightloss so I started to starve myself. I was weak for a long time. One day my mum noticed that I had stopped eating so she forced me to eat. No-one wants to see their daughter starve themselves. In secondary school I was quite normalweight because of my height. My weight started to gradually rise and by the winter of 8th grade I was nearly 100kg (220lbs) and my height was 172cm (5'7). I absolutely hated myself. I cried everytime I had to look in the mirror. Nothing fit. My mum saw me crying about it once and had a peptalk for me. She helped me start my weightloss.

 I joined the gym eventhough I was too young for that. Most gyms only accept 16+. Our school nurse wrote me a remission to start at a gym because my weight was a risk for my health. My weight started to drop. I got muscles. I went to the gym with my mum and I was motivated. By the spring of 8th grade I had lost 15kg (33lbs). It was noticeable. Everyone talked about it at school and I had such a good self-esteem. My instagram followers rose and people started talking to me and I was more involved in things. People talked behind my back about my weightloss and I was often told that I looked great after the weightloss. Smaller clothes fit me. My stamina got better and my P.E. grades rocketed so that I was one of the top ones in that class. Then I made the mistake. I thought that I could stop with my diet and that I couldn’t gain back my weight that easily. Now I weigh 89kg (196lbs) and I feel worse than before. Because I know that I failed and it was all for nothing. I decided to start again.

It starts today. With you.

~With love, your little Donut.

[aridara]

BMI only look sat the relation of height and weight so it's not accurate. But the thing is... it's not incorrect in the way you may think. BMI actually OVERestimates people's health. If your BMI tells you you're normalweight, then there's still a good chance you have too much fat. However, if your BMI tells you you're overweight or obese, then there's only a very slight chance that you don't have too much fat. Some body builders have high BMIs... yes. So what?Sincerely, a fat person

Again: BMI doesn’t tell you how much fat do you have. It’s not an indicator of fatness. It literally cannot be an indicator of fatness, because fatness isn’t even considered by it.

Moreover: weight has not been an indicator of health.

Lastly: can you tell me why overweight and obese people tend to live longer than “normal” weight people, once you’ve considered equal medical treatment* and diabetes**?

(*: Fat people are overwhelmingly more likely to have their medical doctors dismissed by a doctor as “too much weight”, regardless of whether it’s the acutal cause of their health issues or not.)(**: Diabetes type 2 causes weight gain. It’s not caused by being overweight.)

[recovery-anorexia]

Good Morning

[taliemsite-blog]

The mechanical behavior of concrete materials is strongly influenced by its microstructure. The macroscopic properties of concrete materials such as strength and stiffness are dependent on the properties micromechanics. The advance of composite mechanics and advanced  computing technologies has made possible the micromechanical analysis of concrete materials.. In the first status of micromechanical modeling with special emphasis on the advantage and disadvantage of each model is presented. The current paper focuses on the geometrical  description and numerical simulation of normalweight concrete at the mesoscale. In the first part the numerical representation of concrete at  the mesoscale is introduced. The internal structure of concrete is considered at the micro level, and is treated as a three phase material  comprised of aggregate particle, matrix, and the aggregatematrix interfaces The generation of the mesoscale geometry, the finite element  discretisation and the applied material laws Whit micro plane theory are described. The main objective of this paper is to investigate the  macroscopic behavior and Progressive failure of concrete materials under static loading, as influenced by the properties of its constituents at the meso level.

[everythingspoiler]

#Overweight #Underweight #Migraine #BMI #NormalWeight #Weight https://t.co/hXzYSdDZz0

http://twitter.com/euneedspoiler