Refined lardRefined lard is pork fat rendered from adipose tissue and subsequently purified (filtration, bleaching, deodorization, and clarification) to deliver a neutral flavor and reliable cooking performance. Primary sources are backfat and perirenal “leaf lard,” the latter prized for fine pastry applications due to its plasticity an... (Read the full Tiiip)
Refined lardRefined lard is pork fat rendered from adipose tissue and subsequently purified (filtration, bleaching, deodorization, and clarification) to deliver a neutral flavor and reliable cooking p ...
Refined lard is pork fat rendered from adipose tissue and subsequently purified (filtration, bleaching, deodorization, and clarification) to deliver a neutral flavor and reliable cooking performance. Primary sources are backfat and perirenal “leaf lard,” the latter prized for fine pastry applications due to its plasticity and clean taste.
Caloric value (dry product, 100 g) Approximately 880–902 kcal per 100 g (typical ≈ 900 kcal/100 g; energy almost entirely from lipids).
Composition and fatty acid profile (indicative, % of total fat) SFA: ~35–42% (palmitic ≈ 22–26%; stearic ≈ 10–15%). MUFA: ~40–50% (oleic predominant). PUFA: ~8–15% (linoleic prevalent; ALA in traces). Cholesterol: ~80–100 mg/100 g (varies with tissue, breed, and diet).
Technological and sensory properties Refined lard has a neutral to mildly meaty aroma; its semi-solid state at room temperature and tendency to crystallize in β′ form support lamination and tenderness in doughs (pies, pastries, flatbreads). The smoke point typically ranges ~190–205 °C, suitable for moderate frying and sautéing; repeated high-heat use accelerates oxidation and secondary compound formation. Oxidative stability is intermediate: lower than more saturated animal fats but higher than oils rich in PUFA. Absence of proteins and sugars limits Maillard darkening compared with unclarified fats during frying.
Manufacturing process (outline) Adipose raw material is gently rendered under controlled oxygen exposure, then filtered to remove cracklings and fines. Subsequent bleaching/deodorization standardizes color and aroma; some lines apply physical fractionation to tune plasticity and SFC profile. Approved antioxidants may be added, where permitted, to retard rancidity.
Food applications Refined lard is traditional in laminated and enriched doughs, regional breads, shortcrusts, biscuits/crackers, and fried products. In cooking it serves for sautés and shallow fries where crispness and neutral flavor are desired. In charcuterie and hot deli items it can act as a confit medium or protective fat cap.
Nutrition and health Refined lard provides concentrated energy and a substantial MUFA fraction (oleic), alongside significant SFA and moderate PUFA. Dietary impact depends on overall substitutions: replacing SFA with MUFA/PUFA generally favors lipid profiles, but net effects are pattern-dependent. Non-hydrogenated lard contains trace TFA; hydrogenation (where used) increases TFA and is best avoided. Ethical/religious dietary frameworks (e.g., kosher/halal, vegetarian/vegan) preclude lard.
Quality and specification themes Appearance: white–ivory; clear when melted; free of particulates. Odor/flavor: neutral; free from rancid or animal off-notes. Free fatty acids and peroxide value: low and stable across shelf life. Functional metrics: smoke point and SFC curve aligned with application. Contaminants: metals/process residues within legal limits; migration compliant for food contact. Supply-chain controls: traceability and conformity under GMP and HACCP plans.
Storage and shelf life Store in opaque, well-sealed containers, cool and protected from light/air and external odors. Shelf life is typically several months at controlled ambient temperature; refrigeration further extends stability. Long-term reuse of frying fat is discouraged because oxidation/polymerization products accumulate and degrade quality and safety.
Troubleshooting Painty/rancid odor: oxidative degradation—improve barrier packaging, FIFO rotation, and storage temperature. Foaming during frying: water/impurities or thermal degradation—filter, lower temperature, or refresh the bath. Poor flakiness in pastry: suboptimal crystallization or excessive liquid oil substitution—adjust cooling curve and handling. Residual animal note: inadequate refining/deodorization or mixed raw material—review sourcing and processing.
Sustainability and supply chain Refined lard valorizes a by-product of the pork sector, contributing to whole-animal utilization. Husbandry, feed, and welfare practices influence composition and quality. Used frying fats require authorized collection and recycling; improper disposal should be avoided.
Conclusion Refined lard offers neutral flavor, plastic workability, and dependable frying and baking performance. Careful raw-material selection, tight process control, and proper storage maximize stability, safety, and sensory outcomes across diverse applications.
Mini-glossary SFA — Saturated fatty acids: To moderate; health impact depends on the overall dietary pattern and the replacement nutrient. MUFA — MonoUnsaturated fatty acids: Generally favorable for lipid profile and culinary stability (e.g., oleic acid). PUFA — PolyUnsaturated fatty acids: Beneficial but more oxidation-prone; include omega-6 (linoleic) and omega-3 families. ALA — Alpha-linolenic acid (omega-3): Present only in traces in lard; more abundant in certain vegetable oils. TFA — Trans fatty acids: To avoid; industrial hydrogenation raises TFA levels and cardiometabolic risk. SFC — Solid fat content: Fraction of fat solid at a given temperature; key for plasticity and pastry performance. GMP — Good Manufacturing Practice: Codified procedures and controls ensuring hygiene, consistency, traceability, and quality. HACCP — Hazard Analysis and Critical Control Points: Preventive food-safety system defining hazards, CCPs, limits, monitoring, corrective actions, and verification. FIFO — First in, first out: Inventory rotation principle—use oldest lots first to preserve quality and safety.
Warning:
in 100 grams of lard there are 95mg of cholesterol.
100 grams of lard provide ≈ 895 kcal.
Animal studies establishing a relationship between heavy lard consumption, obesity(1) and cardiovascular inflammation (2).
Other studies have shown that significant intakes of lard in the diet have led to increased prostate volume (3), breast cancer(4) and pancreatic problems(5).
Lard, like margarine, is a major source of trans-fatty acids and saturated fatty acids. The association between these fats and a high risk of cardiovascular disease has been widely demonstrated. Moreover, animal models with high fat content represent the classic and most common method to study obesity. The results of this study showed that a high dietary intake of margarine and lard could induce a specific inflammation of the deposit with a reduced expression of anti-inflammatory type M2 adipose tissue in white adipose tissues (6).
(1) Wang X, Cheng M, Zhao M, Ge A, Guo F, Zhang M, Yang Y, Liu L, Yang N. Differential effects of high-fat-diet rich in lard oil or soybean oil on osteopontin expression and inflammation of adipose tissue in diet-induced obese rats. Eur J Nutr. 2013 Apr;52(3):1181-9. doi: 10.1007/s00394-012-0428-z.
Abstract. Purpose: To examine the effect of different dietary fat types on osteopontin (OPN) expressions and inflammation of adipose tissues in diet-induced obese rats. Methods: Male Sprague-Dawley rats were randomly assigned to one control group fed standard diet (LF, n = 10) and two high-fat diet groups fed isoenergy diet rich in lard or soybean oil (HL or HS, n = 45 each). Diet-induced obese rats in HL and HS group were then subdivided into two groups either continuously fed high-fat diet or switched to low-fat diet for 8 more weeks. Fasting serum glucose, insulin, and OPN concentrations were assayed and QUICKI was calculated; the expression of OPN, IL-6, IL-10, TNF-α, NF-κB, and F4/80 in adipose tissue was determined. Results: Both high-fat diets lead to comparable development of obesity characterized by insulin resistance and adipose tissue inflammation. Obese rats continuously fed high-fat diet rich in lard oil exhibited the highest fasting serum insulin level and adipose tissue OPN, F4/80, TNF-α, and NF-κB expression level. In both high-fat diet groups, switching to low-fat diet resulted in less intra-abdominal fat mass, decreased expression of F4/80, TNF-α, and NF-κB, while decreased OPN expression was only observed in lard oil fed rats after switching to low-fat diet. Conclusions: Reducing diet fat or replacing lard oil with soybean oil in high-fat diet alleviates obesity-related inflammation and insulin resistance by attenuating the upregulation of OPN and macrophage infiltration into adipose tissue induced by high-fat diet.
Abstract. Obesity has reached epidemic proportions worldwide. Several animal models of obesity exist, but studies are lacking that compare traditional lard-based high fat diets (HFD) to "Cafeteria diets" (CAF) consisting of nutrient poor human junk food. Our previous work demonstrated the rapid and severe obesogenic and inflammatory consequences of CAF compared to HFD including rapid weight gain, markers of Metabolic Syndrome, multi-tissue lipid accumulation, and dramatic inflammation. To identify potential mediators of CAF-induced obesity and Metabolic Syndrome, we used metabolomic analysis to profile serum, muscle, and white adipose from rats fed CAF, HFD, or standard control diets. Principle component analysis identified elevations in clusters of fatty acids and acylcarnitines. These increases in metabolites were associated with systemic mitochondrial dysfunction that paralleled weight gain, physiologic measures of Metabolic Syndrome, and tissue inflammation in CAF-fed rats. Spearman pairwise correlations between metabolites, physiologic, and histologic findings revealed strong correlations between elevated markers of inflammation in CAF-fed animals, measured as crown like structures in adipose, and specifically the pro-inflammatory saturated fatty acids and oxidation intermediates laurate and lauroyl carnitine. Treatment of bone marrow-derived macrophages with lauroyl carnitine polarized macrophages towards the M1 pro-inflammatory phenotype through downregulation of AMPK and secretion of pro-inflammatory cytokines. Results presented herein demonstrate that compared to a traditional HFD model, the CAF diet provides a robust model for diet-induced human obesity, which models Metabolic Syndrome-related mitochondrial dysfunction in serum, muscle, and adipose, along with pro-inflammatory metabolite alterations. These data also suggest that modifying the availability or metabolism of saturated fatty acids may limit the inflammation associated with obesity leading to Metabolic Syndrome.
(3) Escobar EL, Gomes-Marcondes MC, Carvalho HF. Dietary fatty acid quality affects AR and PPARgamma levels and prostate growth. Prostate. 2009 Apr 1;69(5):548-58. doi: 10.1002/pros.20905. PMID: 19143008.
(4) Di Pietro PF, Medeiros NI, Vieira FG, Fausto MA, Belló-Klein A. Breast cancer in southern Brazil: association with past dietary intake. Nutr Hosp. 2007 Sep-Oct;22(5):565-72.
Abstract. Objective: To determine possible associations between the risk of breast cancer in Brazilian women and demographic, social and economical variables, and past dietary intake. Methods: A case-control study was conducted in Joinville, Santa Catarina, Brazil, between june and november 2003 involving a group of 33 women recently diagnosed with breast cancer and a control group of 33 healthy women volunteers. Personal details, health history and past dietary intake were obtained via questionnaires and interviews. Data between groups were compared using chi2, Fisher, and Student's t test, whilst associations were evaluated using a non-conditional logistic regression method and odds ratio (OR). Results: Statistically significant differences between the two groups were revealed with respect to age distribution (P = 0.007), family income level (P = 0.02), educational level (P < 0.0001) and attainment of menopause (P < 0.0001). After adjustment, with regard to family income level, of the data concerning past dietary intake, the consumption of pig lard (OR = 6.32) and fatty red meat (OR = 3.48) were found to be associated with an increase in the risk of breast cancer. The regular ingestion of apples (OR = 0.30), watermelons (OR = 0.31), tomatoes (OR = 0.16), plain cakes (OR = 0.30) and desserts (OR = 0.20) afforded some degree of protection against the development of the disease. Conclusions: Age (> 45 years), low family income (< $520/month), poor educational level (primary school level or lower) and past regular consumption of pork fat and fatty meat may be factors associated with an increased risk of breast cancer.
(5) Zhang XL, Li F, Cui YQ, Liu S, Sun HC, Zhonghua Wai Ke Za Zhi. 2012 Jul;50(7):646-9. The role of oxide stress during the pathogenesis of chronic pancreatic injuries induced by chronic high-fat diets in rat.
Abstract . Objective To provide more detailed information on the roles of lipid peroxidation in the pathogenesis of chronic pancreatic injuries in a pre-clinical rat model. Methods Totally 72 rats were divided into 6 groups (12 in each group) Rats in 5 experimental groups (n = 12) were fed with a high-fat diet (1% cholesterol, 10% lard, 0.3% sodium tauroglycocholate, 87.3% standard rodent chow as the control group) for 2, 4, 6, 10 and 16 weeks, respectively. Morphological studies in the pancreas tissue samples from rats were investigated by using various histological methods. Pancreatic stellate cells (PSCs) were identified by immunohistochemical staining for Desmin and α-smooth muscle actin (α-SMA). The expression of the lipid peroxidation was detected by immunostaining for 4-hydroxy-2-nonenal (4-HNE) and thromboxane A2 receptor (TxA2r). The co-localization of α-SMA and 4-HNE or α-SMA and TxA2r in PSCs was also analyzed in this study. Results. Pancreatic cells with positive staining for Desmin and α-SMA in HFD rats were distributed in a more extensive way when compared to that in the control group. The levels of pancreatic 4-HNE and TxA2r were increased in rats from HFD groups significantly. The co-localization of 4-HNE and TxA2r were also found within activated PSCs in both of groups. Conclusion. The results showed that a chronic HFD feeding may increase the lipid peroxidation process and collagen synthesis through a critical signaling pathway of activated PSCs following pancreatic injuries in rats.
(6) Wang N, Guo J, Liu F, Wang M, Li C, Jia L, Zhai L, Wei W, Bai Y. Depot-specific inflammation with decreased expression of ATM2 in white adipose tissues induced by high-margarine/lard intake. PLoS One. 2017 Nov 15;12(11):e0188007. doi: 10.1371/journal.pone.0188007.
Abstract. A high-fat diet has been recognized as an important risk factor of obesity, with variable impacts of different fatty acid compositions on the physiological process. To understand the effects of a high-margarine/lard diet, which is a major source of trans fatty acids (TFAs)/ saturated fatty acids (SFAs), elaidic acid as a biomarker of margarine intake was used to screen affected adipokines on mature human adipocytes in vitro. Weaned male Wistar rats were fed a high-fat diet enriched with margarine/lard to generate obesity-prone (OP) and obesity-resistant (OR) models, which were then used to explore the inflammatory responses of depot-specific white adipose tissue. Adiposity, glucose and lipid metabolism parameters and macrophage cell markers were also compared in vivo. In the subcutaneous depot, a high-margarine diet induced elevated IL-6, MCP-1 and XCL1 expression levels in both M-OP and M-OR groups. High-lard diet-fed rats displayed higher protein expression levels of MCP-1 and XCL1 compared with the control group. In the epididymal depot, significantly elevated IL-6 production was observed in M-OP rats, and high-lard diet-fed rats displayed elevated IL-6 and decreased XCL1 expression. In the retroperitoneal depot, a high-margarine diet caused higher IL-6 and MCP-1 expression levels, a high-lard diet caused elevated IL-6 expression in L-OP/L-OR rats, and elevated XCL1 expression was observed only in L-OP rats. In general, CD206 mRNA levels were notably down-regulated by high-fat diet feeding in the above-mentioned depots. CD11c mRNA levels were slightly upregulated in the subcutaneous depot of OP rats fed a high-margarine/lard diet. In the epidydimal depot, higher expression levels of F4/80 and CD206 mRNA were observed only in high-margarine diet-fed OP rats. These results suggest that depot-specific inflammation with decreased expression of adipose tissue anti-inflammatory M2-type (ATM2) macrophages could be induced by high-margarine/lard intake.
Refined lard 
