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ARTICLE

7 Science-Based Health Benefits of Drinking Enough Water

15 Apr 2016

2. Hydration Has a Major Effect on Energy Levels and Brain Function

Your brain is strongly influenced by hydration status.
Studies show that even mild dehydration (1-3% of body weight) can impair many aspects of brain function.

In a study of young women, fluid loss of 1.36% after exercise impaired both mood and concentration, and increased the frequency of headaches.
Another similar study, this time in young men, showed that fluid loss of 1.59% was detrimental to working memory and increased feelings of anxiety and fatigue .
A 1-3% fluid loss equals about 1.5-4.5 lbs (0.5-2 kg) of body weight loss for a 150 lbs (68 kg) person. This can easily occur through normal daily activities, let alone during exercise or high heat.
Many other studies, ranging from children to the elderly, have shown that mild dehydration can impair mood, memory and brain performance .

Bottom Line: Mild dehydration (fluid loss of 1-3%) can impair energy levels and mood, and lead to major reductions in memory and brain performance.

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Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy

29 Feb 2016

Summary. I.V. fluid therapy does not result in the extracellular volume distribution expected from Starling’s original model of semi-permeable capillaries subject to hydrostatic and oncotic pressure gradients within the extracellular fluid. Fluid therapy to support the circulation relies on applying a physiological paradigm that better explains clinical and research observations. The revised Starling equation based on recent research considers the contributions of the endothelial glycocalyx layer (EGL), the endothelial basement membrane, and the extracellular matrix. The characteristics of capillaries in various tissues are reviewed and some clinical corollaries considered. The oncotic pressure difference across the EGL opposes, but does not reverse, the filtration rate (the ‘no absorption’ rule) and is an important feature of the revised paradigm and highlights the limitations of attempting to prevent or treat oedema by transfusing colloids. Filtered fluid returns to the circulation as lymph. The EGL excludes larger molecules and occupies a substantial volume of the intravascular space and therefore requires a new interpretation of dilution studies of blood volume and the speculation that protection or restoration of the EGL might be an important therapeutic goal. An explanation for the phenomenon of context sensitivity of fluid volume kinetics is offered, and the proposal that crystalloid resuscitation from low capillary pressures is rational. Any potential advantage of plasma or plasma substitutes over crystalloids for volume expansion only manifests itself at higher capillary pressures.

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Microvascular fluid exchange and the revised Starling principle

The plasma, interstitial fluid (ISF), and lymph compartments are linked in series and, in the steady state, fluid flows continuously from one compartment to the next. Lymph drains back into the circulation chiefly at the major veins at the base of the neck. Accidental lymphatic fistulae in the neck indicate a total post-nodal lymph flow of up to 4 L/ day in humans. Later work revealed that roughly half the fluid content of afferent lymph can be absorbed by lymph node microvessels,1,2 raising the fluid turnover estimate to !8 L/day.3 This is a considerable fluid turnover; since human plasma volume is only !3 L, the entire plasma volume (except the proteins) leaves the circulation approximately once every 9 h.

Substantial fluid movements between the plasma and interstitium account for the rapid swelling of acutely inflamed tissues (minutes), and for the oedematous swelling of venous thrombosis, cardiac failure, and lymphatic failure over hours to days. Conversely, haemodilution following an acute haemorrhage reveals a rapid absorption of ISF into the blood stream (!0.5 L in 15–30 min). Acute fluid transfers are important medically, because lasma volume is a majordeterminant of the cardiac filling pressure and thus cardiac output (Starling’s ‘law of the heart’).

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Lymphedema: Separating Fact From Fiction

Lymphedema in right arm of patient; from Boris M, et al. Oncology. 11:99-109,1997
The most recent survivorship data from the Surveillance, Epidemiology, and End Results (SEER) database demonstrate a significant increase in the number of US cancer survivors over the last 30 years, from roughly 3 million in 1973 to nearly 12 million in 2008.[1] As a result, issues of survivorship have stimulated new focus for clinical trials, not only to determine the most effective therapeutic regimen (surgery, drug, or radiation) but also to identify the one with the least influence on future quality of life. Lymphedema has long been a feared complication of surgical cancer treatment, and notably one that negatively impacts survivorship. Fear of lymphedema stems from patient concerns regarding the chronic, progressive nature of the condition and the clinician’s relative inability to predict or prevent its development. Furthermore, decades of physician and allied health teachings based on opinion and theory have perpetuated the myths shrouding lymphedema risk, prevention, and treatment.
A vast body of literature documents the occurrence of breast cancer–related lymphedema, with more than 1400 articles indexed in PubMed-MEDLINE databases alone. Importantly, lymphedema also exists after surgery for non–breast-cancer-related malignancies, but data documenting this occurrence are rare in comparison. Recently, Cormier et al found only 47 studies between 1972 and 2008 with more than 10 patients that prospectively evaluated lymphedema as a primary or secondary outcome after treatment for melanoma, bladder, sarcoma, penile, prostate, vulvar, cervical, endometrial, or head and neck cancers.[2] The authors’ analysis of these studies demonstrated the overall incidence of lymphedema to be 16.3% after melanoma, 10.1% after genitourinary cancers, and 19.6% after gynecologic malignancies, and notes that lymphedema rates are higher when the lower rather than upper extremity is affected. Given the abundance of breast cancer data, this review will focus on breast cancer–related lymphedema. However, the principles and controversies discussed are relevant regardless of the type of malignancy to which the lymphedema is attributed.

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The Big Picture: Every thing you wanted to know about lymphoedema

It’s often a surprise for both you and the health professional when a limb begins to show the early warning signs of lymphoedema or actually becomes swollen. It’s difficult to predict the effects of surgery and/or radiotherapy on the lymphatic system and thus whether a limb will swell not only because of anatomical variation between individuals but also as a consequence of other prior events on the local area lymphatic system. However, as the bottom line, if the lymphatic load becomes greater than the lymphatic transport capacity then that area, whether it be associated with a small lymph collector, a whole lymphatic territory or the whole limb, will become swollen.
Some of you may also have had prior damage to their lymphatic system, for instance soft tissue injury, frozen shoulder or problematic hip joint and of course on top of this we have heart and blood vessel issues and thyroid problems, inflammatory events, heritable conditions from your parents and problems with fat deposition and its removal (called Lipoedema – more about that later!), although the latter are primarily confined to the legs.
Being aware of the non-lymphatic side of the problem and directing specific treatment towards them before dealing with the lymphatic system issues is important for you if we are to achieve the best outcome for the specific lymphatic system treatment, which focuses on reducing the load on the remaining lymphatic system and/or improving its transport capacity. (I can’t emphasise the importance of this point too much!) Generally, your main role is in lymphatic load management while the lymphoedema therapist should have their main concerns with improving lymphatic flow and transport.
Once lymphoedema has developed there are no treatment or management miracles, thus prevention though early detection and risk minimisation is crucial. At the moment we do have the knowledge and tools undertake this but there is poor insertion into practice.
Not withstanding this, there are some strong emerging treatment options. Once the problem of lymphoedema or its risk is detected there must be ongoing good communication with the specialist
until you are discharged to the General Practitioner (GP), and then between the GP, the lymphoedema therapist, other members of the multi-disciplinary team and yourself to achieve optimal outcomes. As hard as it sometimes is your compliance is critical if good outcomes are to be attained.

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