Erandio 





ERANDIO ERAIKITZEN 

aza 12 2010

Rechazamos la violencia contra las mujeres

Honek argitaratua: endi ordu honetan: 23:29:47 hemen: Erandio

Queremos sumarnos a la campaña de rechazo a la violencia contra las mujeres y os invitamos a participar en los concursos locales.

El Servicio de Igualdad del Ayuntamiento de Erandio amplia la información sobre el concurso y si el trabajo es seleccionado participará en el I Festival Beldur Barik el 27 de noviembre.

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Etiquetas blog: ea ; Erandio ; Eusko Alkartasuna ; Mujeres ; violencia ;
Etiquetas todos los blogs: ea ; Erandio ; Eusko Alkartasuna ; Mujeres ; violencia ;

29 iruzkinak -> “Rechazamos la violencia contra las mujeres”

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  28. side effects of cjc 1295 and ipamorelinel 25 ira 2025 ordu honetan: 08:47:50

    CJC 1295 Ipamorelin

    CJC 1295 and Ipamorelin

    The combination of CJC‑1295 and Ipamorelin has become a popular strategy for those looking to enhance growth hormone release without the side effects associated with traditional growth hormone therapy.

    These two peptides work synergistically, stimulating the pituitary gland to produce natural
    levels of growth hormone (GH) and insulin‑like growth factor 1 (IGF‑1).

    What are CJC 1295 and Ipamorelin?

    CJC‑1295 is a synthetic analog of growth hormone‑releasing hormone (GHRH).

    It binds to GHRH receptors on pituitary cells, prolonging the release of GH.
    Unlike natural GHRH, CJC‑1295 has a longer half‑life due to its attachment to
    a carrier molecule that protects it from rapid degradation.

    Ipamorelin is a selective growth hormone secretagogue.

    It mimics ghrelin, the “hunger hormone,” but
    specifically targets growth hormone‑secreting cells in the pituitary.

    Ipamorelin’s high affinity for GH receptors leads to a significant rise in circulating GH levels with minimal stimulation of other hormones such as cortisol
    or prolactin.

    How Do CJC 1295 and Ipamorelin Work?

    When administered together, CJC‑1295 provides sustained
    activation of GHRH receptors, creating a baseline increase in GH
    secretion. Ipamorelin then delivers a rapid spike
    by directly stimulating GH release. The dual action results in both a steady elevation of GH
    levels throughout the day and an acute surge after each dose.
    This pattern closely resembles natural circadian hormone rhythms, improving anabolic processes like protein synthesis, fat metabolism, and tissue repair.

    Potential Benefits of CJC 1295 and Ipamorelin

    Muscle growth and recovery – Enhanced protein synthesis supports
    lean muscle gains and faster post‑workout healing.

    Fat loss – Elevated GH increases lipolysis, helping to reduce visceral adiposity
    while preserving muscle mass.

    Improved sleep quality – Growth hormone peaks during deep sleep; these
    peptides can reinforce that natural cycle, leading to
    better rest.

    Joint health – IGF‑1, stimulated by increased GH, promotes cartilage repair and reduces joint stiffness.

    Skin rejuvenation – Collagen production rises with higher IGF‑1 levels,
    resulting in firmer skin and reduced fine lines.

    How to Use CJC 1295 and Ipamorelin

    Typical protocols involve subcutaneous injections. A common regimen is:

    CJC‑1295: 2–3 µg per injection, once daily or every other day, depending on the specific analog
    used.

    Ipamorelin: 100–200 µg per injection, given 30 minutes before
    or after the CJC‑1295 dose to maximize synergistic effect.

    Many users split doses between morning and evening to maintain stable hormone levels.

    It is advisable to cycle usage—often 8–12 weeks on, followed by a break—to prevent desensitization of
    pituitary receptors.

    Considerations and Side Effects of CJC 1295 and Ipamorelin

    While generally well tolerated, some individuals may experience mild side effects such as:

    Injection site soreness or swelling

    Water retention leading to temporary puffiness

    Headaches or dizziness in the initial days of therapy

    Longer‑term use warrants monitoring for potential insulin resistance or increased
    IGF‑1 associated risks. Always consult a healthcare professional
    before starting peptide therapy, especially if you have underlying health conditions.

    Recent Posts

    Should I Wear a Brace After PRP Injections?

    PRP for Shoulder Pain

    PRP For Shoulder Labrum Tear

  29. sustanon 250 deca durabolin dianabol cycleel 26 ira 2025 ordu honetan: 17:35:19

    Anabolic Steroid Wikipedia

    Short‑answer:

    There isn’t a magic “X‑day” after which you can stop looking at your weight.
    Progress is usually assessed every 4–6 weeks (about a month or so), but you’ll want to see consistent
    trends over several weeks before deciding whether to keep going,
    adjust your plan, or take a break.

    Why the 4–6‑Week Window Makes Sense

    Factor How it affects timing

    Body‑fat changes Reducing fat takes time. A realistic drop is ~0.5 lb per week of caloric deficit.

    In 4–6 weeks you’ll see a measurable change.

    Water weight & glycogen Fluctuations happen daily; the first few weeks are often dominated by water shifts, not true fat loss.

    Metabolic adaptation The body may slow its metabolism after
    several weeks of calorie restriction. Seeing how your weight
    responds over 4–6 weeks helps spot this trend early.

    Hormonal response Hormones (insulin, cortisol, leptin) stabilize over a few weeks; sustained changes in these levels are reflected in longer-term trends.

    > Bottom line: A single day’s number can be misleading because
    of daily variations. Looking at 4–6 week data gives you a clearer picture of whether your
    calorie deficit is producing sustainable fat loss.

    3️⃣ How to Use This Information

    Step What to Do Why It Matters

    1. Record daily calories Log all foods, drinks, and snacks
    in an app (MyFitnessPal, Cronometer). Accurate data is the foundation for analysis.

    2. Track weight & body composition weekly Weigh
    yourself once a week at the same time of day; if possible, use DEXA or skinfold calipers to monitor fat mass vs muscle.
    Prevents short‑term fluctuations from skewing your view.

    3. Plot calorie intake vs weight trend Use spreadsheet software to overlay daily calories on weight changes over 30 days.
    Visual patterns emerge—e.g., weight plateau after certain calorie level.

    4. Identify “threshold” points Look for ranges where increasing calories by 100–200 kcal/day no longer produces weight gain; this likely
    reflects your energy requirement. This is the dynamic of energy balance in real life.

    5. Refine and re‑test Adjust calories upward or downward based on identified threshold, then repeat a new month to confirm consistency.
    Repetition confirms that the threshold is stable over
    time.

    Practical Example (Hypothetical)

    Week Avg Daily Calories Weight Change

    1 2,200 kcal +0.5 kg

    2 2,300 kcal +0.8 kg

    3 2,400 kcal +0.9 kg

    4 2,500 kcal +1.2 kg

    The weight gain slows in week 4 relative to earlier weeks.
    You might deduce that your maintenance level is around 2,400–2,500 kcal.

    Confirm this by repeating with a different dataset or adjusting for activity changes.

    5. Why the “Average Calorie Intake” Approach Is Wrong

    Assumes Perfect Balance: The approach presupposes that all calories you eat are stored as fat, ignoring metabolic processing.

    Ignores Variable Energy Expenditure: Your basal metabolic rate and activity level change daily; a static average intake cannot
    capture this dynamic.

    Disregards Time‑Scale Effects: Over weeks or months,
    the body’s storage and mobilization of energy buffer short‑term fluctuations.
    An average does not reflect cumulative excesses or deficits.

    In essence, the average calorie approach conflates
    two distinct processes—calorie consumption (input) and body weight
    change (output)—and equates them directly without considering the intermediary metabolic steps.

    4. A More Plausible, Mechanistic Model

    Below is a concise outline of a model that links diet to weight using physiological principles rather than a simplistic average:

    Component Description Key Equations / Concepts

    Energy Intake (EI) Calories consumed per day. \( EI = \sum_food C_i \)

    Basal Metabolic Rate (BMR) Energy expended at rest. Harris–Benedict, Mifflin‑St Jeor,
    or measured via indirect calorimetry.

    Thermic Effect of Food (TEF) ~10% of EI for protein; varies by macronutrient.
    \( TEF = 0.1 \times EI_protein + 0.05 \times EI_fat + 0.03 \times EI_carb \)

    Physical Activity Energy Expenditure (PAEE) Calories burned during activity;
    measured via accelerometry or heart‑rate monitors.

    Total Daily Energy Expenditure (TDEE) \( TDEE = TEE + TEF +
    PAEE \).

    Energy Balance \( EB = EI - TDEE \); positive EB leads to fat
    gain (~3500 kcal ≈ 1 lb fat).

    This framework is used by dietitians and researchers to estimate
    how many calories a person can eat or must restrict to achieve weight loss.

    4. How the Body Uses Food for Energy

    Nutrient Main Pathway Primary Product

    Carbohydrates Glycolysis → Pyruvate →
    Acetyl‑CoA (via PDH) → TCA cycle → ATP (via ETC). Glucose or glycogen stores.

    Fats β‑oxidation → Acetyl‑CoA + NADH/FADH₂ → TCA cycle
    → ATP. Triglycerides stored in adipose tissue; also from dietary oils.

    Proteins Deamination → α‑ketoglutarate or other intermediates → entry
    into TCA sustanon 250 deca durabolin dianabol cycle
    (anaplerosis). Dietary amino acids or muscle protein breakdown.

    Efficiency: Fat yields ~9 kcal/g, carbohydrate ~4 kcal/g; proteins also
    provide 4 kcal/g but are not primarily used for energy.

    Regulation: Insulin promotes storage (fatty
    acid synthesis), glucagon promotes mobilization (lipolysis) and gluconeogenesis.

    Summary

    Blood glucose is the main fuel that circulates in the blood.

    The brain can use glucose, lactate, or ketone bodies, but it cannot produce
    its own glucose; any glucose must come from dietary intake or hepatic synthesis.

    If carbohydrate intake is insufficient and the liver is deprived of glycogen (e.g.,
    after a prolonged fast), the brain’s glucose supply
    falls below critical levels (~45 mg/dL).
    The body then switches to ketone bodies for fuel.

    During a 36‑hour fast with no carbohydrate or protein, the blood glucose level can drop
    close to 50–60 mg/dL before ketogenesis compensates.

    These points summarize how the brain obtains energy during fasting and how it
    responds when carbohydrate availability is low.

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